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The coexistence of degenerative spine disease and hip osteoarthritis (OA) is one of the most commonscenarios of Hip Spine Syndrome (HSS). Usually, when a patient with an HSS is referred to surgery, twoseparate treatments are considered for the hip and spine in two different hospitalization steps. We presenta novel strategy of HSS treated simultaneously with an anterior lumbar interbody fusion (ALIF) and atotal hip arthroplasty (THA) through an anterior minimally invasive surgery (AMIS). A simultaneousminimally invasive L5-S1 ALIF and an anterior minimally invasive total hip arthroplasty. (AMIS-THA)was performed on a 48-year-old man with left hip OA, and previous failed L5-S1 posterior instrumentedsurgery resulted in non-union and residual spinopelvic mismatch. A specific blended analgesic protocol(epidural injection plus deep sedation) was applied. Radiological evaluation showed improvement of L5-S1lordosis from 10° preop to 22° postop. Intraoperative total blood loss was 250 ml, and total surgical timewas 120 minutes. Four hours after surgery, the patient showed full ability to walk without crutches. Hewas discharged on post-operative day three. As far as we know, this is the first described case in which HSShas been treated with simultaneous single surgical step by two anterior minimal invasive approaches. Itwas planned to avoid a delay in one of the surgical procedures and to set the hip appropriately for the newlordosis, restoring the ideal spino-pelvic alignment and the hip’s full range of motion.
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OBJECTIVE: To study the early application value of pulmonary ultrasound combined with arterial blood gas analysis in emergency patients with multiple severe injuries complicated by respiratory failure.METHODS: Eighty-one patients with multiple severe injuries complicated by respiratory failure treated in the intensive care unit of the emergency department of our hospital between January 2020 and January 2021 were retrospectively analyzed. According to the different examination methods, the patients were divided into three groups (n = 21), diagnosed only using pulmonary ultrasound (group A), diagnosed only using arterial blood gas analysis (group B), and diagnosed using pulmonary ultrasound combined with arterial blood gas analysis (group C). The initial diagnosis time, diagnosis time, and correct treatment time for patients in each group were recorded. The diagnostic rates of bedside pulmonary ultrasound, blood gas analysis, and bedside pulmonary ultrasound combined with blood gas analysis were compared. Patients were divided into a survival group (n = 65) and a death group (n = 16), and the predictive effect of pulmonary ultrasound on the long-term prognosis of patients was analyzed.RESULTS: The initial diagnosis, diagnosis, and initial correct treatment times in groups B and C were significantly shorter than those in group A, and the initial diagnosis time, diagnosis time, and initial correct treatment time in group C were significantly shorter than those in group B (P < 0.05). The diagnosis rate of the examination method in group A was significantly lower than that in groups B and C (P< 0.05). The lung ultrasound (LUS) score in the survival group was significantly lower than that in the death group, while the right diaphragm displacement, left diaphragm displacement, and average diaphragm displacement in the survival group was significantly higher than those in the control group (P < 0.05). The LUS score in the survival group was significantly lower than that in the death group, while the right diaphragm displacement, left diaphragm displacement, and average diaphragm displacement in the survival group was significantly higher than those in the control group (P<0.05). The receiver operating characteristic curve results showed that right diaphragm displacement, left diaphragm displacement, and average diaphragm displacement had good predictive value.CONCLUSION: Pulmonary ultrasound combined with arterial blood gas analysis is of significant value in the early assessment of patients with multiple severe injuries complicated by respiratory failure and has important clinical significance in the timely treatment and prediction of patient prognosis.
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OBJECTIVE: This study aimed to elucidate the molecular mechanism of N6-methyladenosine (m6A)regulation in lung adenocarcinoma (LUAD) development.METHODS: Gene expression profiles were derived from the TCGA and GEO databases. Theexpression levels of m6A regulators in LUAD and normal tissues were assessed. Consensus clustering wasconducted for differential tumor subtypes. m6A regulators related to prognosis were screened using theLASSO algorithm. A score (RS) system was constructed and verified. The correlation between the riskscore signature, prognosis, and immune cell infiltration was further analysed.RESULTS: We identified the modification features of m6A regulators in LUAD and found that 16m6A genes were aberrantly expressed in tumor tissue compared with normal tissue. Six optimised m6Aregulators, including FTO, RBM15B, and RBMX, were obtained to construct a risk score system. Moreimportantly, the AUC values of the ROC curve were 0.790, 0.729, 0.776, and 0.765 for the four datasets,indicating high predictive ability. Patients in the high-risk group had worse prognoses than those in thelow-risk group (P <0.05). Three clinical factors (RS status, pathological stage, and tumor recurrence)correlated independently with survival outcomes. The proportions of the four immune cell types showedabnormal changes in the two risk groups. The m6A regulatory signature was significantly related toinfiltration by immune cells, such as B cells, CD4+ and CD8+ T cells, and neutrophils (P <0.05).CONCLUSION: We demonstrated the potential roles of six m6A regulators in LUAD progression andimmune cell infiltration. The risk score signature may serve as a reliable tool for prognosis prediction andmay provide effective guidance in LUAD therapy.
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OBJECTIVE: To explore the efficacy of robotic-assisted, laparoscopic and abdominal sacrocolpopexy in treating high-stage pelvic organ prolapse.METHODS: A retrospective multi-centre study was performed. From January 2013 to December 2020, female patients who underwent abdominal sacrocolpopexy (ASC), laparoscopic abdominal sacrocolpopexy (LASC) or robot-assisted abdominal sacrocolpopexy (RASC) in three medical centres of Chinese PLA General Hospital were included. Clinical data were collected, and all patients were followed up for more than 12 months. Anatomic POP-Q were recorded to evaluate the pelvic floor level. In addition, pelvic Floor Distress Inventory-20 (PFDI-20), Pelvic Floor Impact Questionaire-7 (PFIQ-7) and Patient Global Impression of Improvement (PGI-I) were used to evaluate the life quality after surgery.RESULTS: Sixty-nine cases were enrolled in this study, including 35 undergoing ASC, 10 undergoing LASC and 24 undergoing RASC. Patients in ASC (56.3±7.2) were younger than those in LASC (62.2±8.0) and RASC (64.3±10.4). During surgery, the blood loss in ASC (244.9±216.6 ml) was significantly more than in LASC (126.3 ± 84.6 ml) and RASC (62.9 ± 77.5 ml). And RASC (149.0±43.6 min) had a significant advantage in operating time over ASC (188.9 ± 55.8 ml) and LASC (185.5 ± 44.4 ml). There was no intraoperative complication in three groups. In the POP-Q follow-up, postoperative Aa, Ba, Ap, Bp in all groups were significantly improved than the baseline (P<0.05). The objective and subjective cure rates were all 100%. PGI-I score was satisfying (1-2). Postoperative PFDI-20 and PFIQ-7 decreased dramatically after surgery in three groups (P<0.05). Mesh exposure occurred in 10 cases (5 in ASC, 1 in LASC, 4 in RASC, P>0.05) at 2-12 months and were less than 1cm in 8 cases (2A/T3/S1), 1-2cm in 2 cases (3B/T3/S1). The mesh exposures healed after estrogen local application without readmission for surgery.CONCLUSION: RASC showed some advantages over LASC and ASC. It can be recommended in sacrocolpopexy with or without hysterectomy.
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OBJECTIVE: To investigate the role and mechanism of the CD36/FAK/mTORC1 pathway in expressing inflammatory cytokines induced by lipopolysaccharide (LPS) in human mammary epithelial cells (MCF-10A).METHODS: Cells were infected with Escherichia coli using LPS, and the expression of CD36, activation of the FAK/mTORC1 pathway and secretion of inflammatory cytokines were measured. The cell membrane receptors CD36 and TLR4 were subsequently blocked with anti-CD36 and anti-TLR4, and the activation of the CD36/mTORC1 pathway was assessed. The expression of inflammatory cytokines and the activation of the FAK/mTORC1 pathway in LPS-treated cells were evaluated after FAK signal inhibition using TAE226, a specific chemical inhibitor of FAK. The expression of inflammatory cytokines and the activation of the mTORC1 pathway in cells treated with or without LPS were also evaluated after mTORC1 signal inhibition using RNAi.RESULTS: Western blot revealed that CD36 expression was significantly elevated at the mRNA and protein levels after treatment with LPS (p<0.05), and the activation of the FAK/mTORC1 pathway and related transcription factors was notably increased (p<0.05). ELISA showed an increase in the number of inflammatory cytokines TNF-α and IL-6 (p<0.05). The levels of phosphorylated FAK, S6 and 4EBP1 in LPS-stimulated cells were significantly attenuated (p<0.05) when CD36 was blocked compared to the levels in the control group. Further, the levels of phosphorylated FAK, S6, 4EBP1 and STAT1 decreased significantly when CD36 and TLR4 were blocked compared to the levels in the control group. TAE226 remarkably inhibited the activation of the FAK/mTORC1 pathway and the expression of inflammatory cytokines induced by LPS stimulation (p<0.05). The RNAi method was used to alter the expression of the key component of mTORC1, Raptor. The results were consistent with previous findings in Rapamycin-treated cells, in which the mTORC1 pathway was weakened, and the levels of TNF-α and IL-6 decreased.CONCLUSION: CD36 is a co-receptor for LPS and binds to mTORC1 and FAK to form the CD36/FAK/mTORC1 pathway.
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OBJECTIVES: This study aimed to investigate the correlation between apolipoprotein E (ApoE) genepolymorphism and the lipid-lowering effects of the statins rosuvastatin and atorvastatin to provide alaboratory basis for rational clinical drug use.METHODS: A total of 146 patients using rosuvastatin calcium tablets (68 females and 78 males,with a mean age of 61.63 ± 7.32 years) and 114 patients using atorvastatin calcium tablets (51 femalesand 63 males, with a mean age of 64.15 ± 7.93 years) were selected for this study. A real-time fluorescentpolymerase chain reaction was performed to detect ApoE genotypes in patients. In addition, the directclearance method detected total serum cholesterol (TC) by enzyme colorimetry and serum low-densitylipoprotein cholesterol (LDL-C).RESULTS: After treatment with Rosuvastatin as lipid-lowering therapy, there was no significantdifference (P > 0.05) in serum TC and LDL-C levels between patients with E2/E3 and E3/E3 genotypes,but levels were significantly lower (P<0.05) in those patients than in those with the E3/E4 genotype. Forthe patients treated with atorvastatin as lipid-lowering therapy, there were significant differences (P< 0.05)in serum TC and LDL-C levels among the three genotypes, with levels lowest in patients with the E2/E3genotype. For patients with the E2/E3 genotype, there were significant differences (P< 0.05) in serum TCand LDL-C levels between the rosuvastatin and atorvastatin groups. There was no significant difference (P> 0.05) in serum TC and LDL-C levels between the rosuvastatin and atorvastatin groups for patients withE3/E3 and E3/E4 genotypes.CONCLUSION: The ApoE gene may be polymorphic, and this gene polymorphism is correlated withthe lipid-lowering effects of statins. Rosuvastatin and atorvastatin have better lipid-lowering effects in E2/E3 patients and E3/E3 patients than in E3/E4 patients.
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BACKGROUND AND OBJECTIVE: The dysfunction of vascular smooth muscle cells (VSMCs)contributes to the pathogenesis of atherosclerosis, which is associated with coronary heart disease and acutemyocardial infarction (AMI). This study is conducted to explain the biological function of prostaglandin Ereceptor 3 (EP3) in regulating the phenotypes of VSMCs.MATERIALS AND METHODS: Platelet-derived growth factor-BB (PDGF-BB) was used to treatVSMCs to construct the cell model. qPCR was performed to examine the expression of EP3 in the VSMCsafter PDGF-BB treatment. After EP3 was silenced, inhibited or overexpressed in VSMCs, CCK-8 assay,BrdU assay, flow cytometry and Transwell assay were performed to detect the viability, proliferation, cellcycle progression and migration of VSMCs. In addition, the expression levels of PI3K, p-p85, Akt, p-Aktin VSMCs was measured by Western blotting.RESULTS: The expression of EP3 in VSMCs is promoted by PDGF-BB treatment in a time- and dosedependentmanner. EP3 overexpression facilitates the viability, proliferation and migration of VSMCswhile silencing EP3 or pharmacological inhibition of EP3 represses the dysfunction of VSMCs inducedby PDGF-BB. EP3 promoted phosphorylation of p85, Akt (Ser473) and Akt (Thr308) in VSMCs, and thepromoting effects of EP3 on the viability, proliferation, migration and cell cycle progression of VSMCswere counteracted after PI3K signalling was inhibited.CONCLUSION: EP3 participates in inducing the dysfunction of VSMCs induced by PDGF viaregulating PI3K/Akt pathway, suggesting EP3 is a therapeutic target for atherosclerosis, AMI and othercardiovascular diseases.
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Introduction: Baldness is a current problem in aesthetic medicine. This cosmetic defect can lead to serious psychological and emotional stress. Most of the time, the solution to this problem consists of removing or attenuating its cause: alopecia. Among the current hair restoration technique to treat alopecia, one is the biocompatible artificial hair implant.Materials and Methods: The certified medical device used for this study is the biocompatible artificial hair Biofibre4.0. The clinical study was done by collecting clinical data from 18 clinics located in 15 different countries and 4 continents to evaluate the efficacy, safety, and performance of a new artificial hair device generation compared to previous artificial hair. Automatic and manual implanter were utilized by doctors participating in these trials. A new needle material was also used for this study. The standard medical protocol was applied with some differences in the doctor’s personal experience, patient’s situation, and climate.Results: The data collected show that in a sample of about 1337 patients treated in 2020/2021, inflammation and infections are around 7%, and curling is<1%. There were no phenomena of fibre breakage. Itching appeared in about <3% of cases. The problems encountered in most cases were mild and resolvable with appropriate therapy, and only in rare cases (<1%) it was necessary to proceed with the total removal of the fibres. In some cases (<1%), it was just necessary to partially extract the fibres that cause recurrent discomfort for the patient. In most patients, satisfaction was 96%. The limitations in patient movement and lowering of the immune response in many of them caused by COVID SARS 2 might partially affect the final data.Conclusion: This surgery does not imply scar formation and hospitalization. It can be used alone or with other treatments to provide psychological benefits and improve quality of life. Indications are poor donor area, request for immediate aesthetic result and scarce trauma. Patient selection, respect for medical protocol and proper aftercare must be complied with. Contraindicated cases must be avoided, and partial or total removal of fibres is required in case of recurrent problems. Additional improvements to this technique are expected to enable an ever vaster application.
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Objective: The present study aims to observe the effects of Luofengning No. 2 on cardiac function, histopathology, and the transforming growth factor-β (TGFβ)/Smads pathway in rat models.Methods: A post-myocardial infarction heart failure (HF) model was constructed, and a total of 50 male Sprague Dawley rats were randomly divided into six groups: (1) the model group (n = 6), (2) the captopril group (n = 6), (3) the low-dose Luofengning No. 2 group (n = 6), (4) the medium-dose Luofengning No. 2 group (n = 7), (5) the high-dose Luofengning No. 2 group (n = 6), and (6) the sham operation group (n = 5). The serum N-terminal pro-brain natriuretic peptide (NT-proBNP) levels were detected using the enzyme-linked immunosorbent assay, and myocardial fibrosis (MF) was observed through Masson staining. In addition, the collagen volume fraction (CVF) was calculated, and the myocardial tissue TGFβ1, Smad2/3, collagen type I (Col-I), and collagen type III (Col-III) protein expressions were detected using Western blot testing.Results: The general conditions of the rats in the drug administration groups were improved, and the heart weight index, left ventricular weight index, and serum NT-proBNP levels were significantly lower compared with the model group (p<0.05 or p<0.01). Furthermore, the TGFβ1, Smad2/3, Col-I, collagen type III (Col-III), and CVF protein levels in the drug administration groups were significantly lower compared with the model group (p<0.05 or p<0.01). There existed no statistically significant differences in NT-proBNP levels; TGFβ1, Smad2/3, Col-I, and Col-III protein levels; or MF degrees between the captopril group and the high-dose Luofengning No. 2 group (p>0.05).Conclusion: Luofengning No. 2 might positively affect cardiac function and anti-MF improvement in rats with HF; this could be related to TGFβ1/Smad2/3.
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BACKGROUND: Abernethy malformations are rare congenital vascular malformations defined by diverting portal blood away from the liver. We present a case of Abernethy malformation that started with hypersplenism.CASE DISCUSSION: A 44-year-old female had leukopenia and thrombocytopenia 14 years ago and was diagnosed with hypersplenism without manifestations of cirrhosis. Since then, the disease gradually progressed, and the number of erythrocytes, leukocytes, and platelets significantly decreased. In addition, liver perfusion was insufficient for an extended period due to portosystemic shunt, and abnormal liver function was observed. The laboratory investigation excluded viral, alcoholic, drug, and autoimmune factors; magnetic resonance imaging and colour ultrasonography revealed a splenorenal shunt, and type II Abernethy malformation was considered. After shunt ligation, the leukocyte and platelet counts and haemoglobin level quickly returned to normal values, improving liver function. In this report, we discuss the common clinical manifestations, associated anomalies, diagnostic workup, and treatment options of this disorder.CONCLUSION: Abernethy malformation is a rare congenital vascular malformation. This vascular abnormality’s clinical importance and manifestations range from asymptomatic cases to liver or metabolic dysfunctions of various degrees. Treatment strategies are decided according to shunt types, locations, symptoms, severities, and clinical course shunt closure should be advised to cure or prevent complications for type II Abernethy malformation. Long-term follow-up is indicated for all patients.
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OBJECTIVE: The present study aimed to functionally investigate the protective effects and potential mechanisms of action of ISO (Isoquercitrin) in diabetic nephropathy using in vivo and in vitro experiments.METHODS: The mRNA and protein expression levels of markers of fibrosis and inflammation, including TGF-β1, Collagen 1, PAI-1, IκBα, NF-κB, and p-NF-Κb, were analyzed by reverse transcription-PCR analysis and western blotting. In addition, histopathological examination was used to confirm the renal injury. ELISA was used to measure biochemical markers of renal injury, including TNF-α, IL-1β, adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1).RESULTS: Our study demonstrated that ISO decreased the levels of glucose, urinary protein, serum creatinine and blood urea nitrogen and alleviated the histopathological abnormalities in the kidney of rats with streptozocin (STZ)-induced D.N. ISO also suppressed STZ-induced activation of NF-κB signalingpathway and decreased the STZ-induced increase in the levels of the markers of fibrosis and inflammatory response, including TGF-β1, collagen I, plasminogen activator inhibitor-1, TNF-α, IL-1β, ICAM-1 and VCAM-1 in D.N. rats. ISO also exerted similar protective effects on high glucose (H.G.)-treated HK-2 cells. Finally, exogenous TAK-242, a selective inhibitor of Toll-like receptor 4 (TLR4), enhanced the protective effects of ISO on HG-treated HK-2 cells.CONCLUSION: In summary, our study demonstrated that ISO alleviates D.N. by suppressing fibrosis and inflammatory responses. The protective effects seem to be mediated by inhibiting the activation of the TLR4/NF-κB signaling pathway. Our data suggest that ISO has promising therapeutic benefits for patients with D.N.
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Acute lung injury (ALI), its severe form, acute respiratory distress syndrome (ARDS), is a clinicalsyndrome characterized by acute hypoxic respiratory failure, bilateral lung infiltration with edema, andnormal cardiac filling pressure. There is no effective treatment for ALI/ARDS, and our understandingof its pathogenesis is partially based on animal models. With the widely use of Lipopolysaccharide (LPS)for bacterial infection-induced ALI, models for a viral infection-induced ALI are relatively rare. Thisstudy established ALI models using Polyinosinic-polycytidylic acid [poly(I:C)] and LPS intra-trachealinstallation, respectively, and systematic evaluations were conducted. Firstly, histological studiesby hematoxylin and eosin (HE) staining showed that poly(I:C) and LPS could induce inflammatorycell infiltration and structural changes. The lung injury was confirmed with the Wet/Dry ratio inboth treatments with a significantly higher ratio in poly(I:C) group. Total protein concentration inBronchoalveolar Lavage Fluid (BALF) from poly(I:C) and LPS treated groups were also significantlyincreased, while more protein concentration in LPS group than that in poly(I:C) group. Flow cytometryshowed that LPS promoted more alveolar neutrophil infiltration than poly(I:C). Secondly, quantitativePCR showed that poly(I:C) treatment promoted more expression of inflammatory factors, IL-1α, IL-6, TNF-α, and ICAM-1, with decreased expression of CCL-2. Finally, lung ventilation experimentsshowed that both poly(I:C) and LPS caused similar lung function loss with increased Newton resistancein poly(I:C) induced lung injury. In conclusion, poly(I:C) and LPS-induced ALIs were systematicallyevaluated, and distinct characteristics were associated with poly(I:C) induced lung injury. Our studiesmay provide the foundation for understanding the viral infection-induced ALI.
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Studies have demonstrated that miRNA-185 may be a promising therapeutic target for NAFLD.However, the underlying mechanisms have not been fully clarified. Autophagy, an evolutionarilyconserved catabolic process, maintains cellular homeostasis under stressful conditions, and it is closelyassociated with metabolic disorders. We previously reported that miR-185 could regulate autophagyfor the first time via decreasing target genes (RHEB and RICTOR). The present study found thatmiR-185-induced autophagy is responsible for triglyceride (TG) accumulation. Firstly, we confirmedthe regulatory relationship between miR-185 and lipid metabolism. Then, we found that nutrientdeprivation upregulated the miR-185 level, which is associated with a remarkable downregulation ofSREBP1C and FASN, as the main genes of TG synthesis, and also RHEB and RICTOR. Furthermore,the downregulated expression levels of SREBP1C and FASN confirmed that nutrient deprivation coulddecrease lipid storage. The downregulated expression levels of RHEB and RICTOR and increasingLC3 II/LC3-I ratio suggested that autophagy plays a role in lipid accumulation. The results highlightedan important potential role for miR-185-induced autophagy in TG accumulation. Additionally, it wasfound that the autophagosome level was upregulated with si-RHEB or si-RICTOR, which was consistentwith the conversion of LC3-I to LC3-II. The downregulated expression levels of SREBP1C and FASNconfirmed that the down-expression of RHEB or RICTOR could decrease TG accumulation. Therefore,the promotion of autophagy may be a promising therapeutic strategy for NAFLD, and miR-185 is apromising miRNA that can be developed and assessed for its significant clinical effects on NAFLD.
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Objective: To explore the relationship between the expression of L-type amino acid transporter 1(LAT1) and pancreatic cancer’s clinical features and prognosis.Methods: The expression of LAT1 in pancreatic cancer and paracancerous tissue was detected in32 patients with pancreatic cancer postoperatively. The patients’ general condition and expression ofCarcinoembryonic antigen (CEA), Carbohydrate Antigen 19-9 (CA19-9), and Ki67 were recorded. Inaddition, the patients’ clinical course was inquired about via telephone calls.Results: The expression of LAT1 in pancreatic carcinomas was positive significantly higher than thatin paracancerous tissues (13/32 vs 0/32, P<0.001). The expression of LAT1 was positively correlated withKi67 expression (r=0.632, P=0.001) and the degree of differentiation significantly (r=0.390, P=0.027), butnegatively correlated with the number of lymph nodes (r=-0.378, P=0.033). Multivariate analysis confirmedthat the expressions of CEA and LAT1 were independent prognostic factors for disease-free survival (DFS)(PCEA=0.015, PLAT1 =0.042). Meanwhile, CEA and CA199 could predict poor overall survival (OS) (P CEA=0.024, PCA19-9=0.040).Conclusion: Overall, LAT1 is related to the degree of proliferation and differentiation of pancreaticcancer. Moreover, while LAT1 and CEA are markers for predicting DFS in pancreatic cancer, LAT1 is notgood at predicting OS.
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Uterine leiomyoma is a benign tumor of the smooth muscle in the uterus, with an incidence of 70%in all women. Numerous studies have shown that CXXC-type zinc finger protein 5 (CXXC5) is involvedin the development of various diseases. However, whether CXXC5 plays a role in the progression ofuterine leiomyoma is unknown. The expression of CXXC5 was evaluated by immunofluorescence (IF),immunohistochemistry (IHC) and western blot analysis, and CXXC5 was shown to be overexpressed inuterine leiomyoma tissues. The elevated expression levels of transforming growth factor-beta (TGF-β)/Smadpathway-related proteins (TGF-β1, p-Smad2 and p-Smad2) and extracellular matrix (ECM) key markers(MMP-2, MMP-9, ADAM10 and ADAM15) were measured through western blot analysis. The proliferationof uterine leiomyoma cells was tested using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assays, IHC staining detected the expression of proliferation marker Ki-67. Results showed thatTGF-β1 promoted the proliferation of uterine leiomyoma cells while silencing RNA and TGF-β1 inhibitorSB431542 suppressed this effect. The expression of ECM accumulation-related proteins collagen IV andfibronectin was examined via western blot analysis and IF staining. CXXC5 attenuation by silencing RNAand TGF-β1 inhibitor SB431542 suppressed TGF-β1-induced ECM accumulation in primary uterineleiomyoma cells. Silencing of CXXC5 and treatment with SB431542 restrained the TGF-β/Smad pathwayin TGF-β1-treated primary uterine leiomyoma cells. CXXC5 inhibition suppressed uterine leiomyoma cellproliferation and ECM accumulation by modulating the TGF-β/Smad pathway.
