Histology and histopathology Vol.36, nº9 (2021)
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- PublicationOpen AccessTensile strain promotes osteogenic differentiation of bone marrow mesenchymal stem cells through upregulating lncRNA-MEG3(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Zhu, Guozheng; Zeng, Canjun; Qian, Yuepeng; Yuan, Song; Ye, Zelin; Zhao, Shanwen; L, RunguangBackground. With the aging of the population, osteoporosis is becoming more and more common. This progressive bone disease increases the risk of fractures and pain and causes serious harm to people's health and quality of life. Several studies, including our previous studies, confirmed that tensile strain can promote bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation in vitro. In this study, we further explored the mechanism by which tensile strain regulates BMSC differentiation. Methods. A device designed by our group was used to apply tensile strain to BMSCs to study the effects of tensile strain on their differentiation. LncRNA-MEG3 overexpression and silencing models of BMSCs were constructed by lentivirus transfection to study the involvement of lncRNA-MEG3. We assessed osteogenic differentiation of BMSCs by alkaline phosphatase (ALP) staining and the expression of Runx2 mRNA and BMP2 mRNA, while adipogenic differentiation was evaluated by oil red staining and the expression of PPARγ mRNA and C/EBPα mRNA. Results. We demonstrated that proper tensile strain can promote osteogenic differentiation of BMSCs while inhibiting differentiation into adipocytes, and simultaneously promote the expression of lncRNAMEG3. The overexpression of lncRNA-MEG3 further promotes osteogenic differentiation of stressed BMSCs and inhibits expression of miR-140-5p; the knockdown of lncRNA-MEG3 induces the opposite effects. Conclusion. Appropriate mechanical stimulation can inhibit the expression of miR-140-5p by promoting lncRNA-MEG3 expression, thereby promoting the osteogenic differentiation of BMSCs. Our results provide a theoretical basis for physical exercise to improve the prevention and treatment of osteoporosis
- PublicationOpen AccessLINC00937 suppresses keloid fibroblast proliferation and extracellular matrix deposition by targeting the miR-28-5p/MC1R axis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Wan, Jing; He, Xiao-Lei; Jian, Qi-Chao; Fan, Zhi-Feng; Shi, Ying; Luo, Long-FeiLong noncoding RNAs (lncRNAs) are the most recently discovered class of noncoding RNAs. LncRNAs play a crucial role in multiple disorders. However, the role and mechanism of action of lncRNAs in keloids remain unclear. Here, qRT-PCR and western blotting assays were performed to determine the expression of genes and proteins, respectively. MTT assays were carried out to measure the proliferation of keloid fibroblasts. In addition, a luciferase activity assay was conducted to investigate the relationships between LINC00937 and miR-28-5p and between miR-28-5p and MC1R. The results showed that LINC00937 and MC1R were decreased, whereas miR-28-5p was increased in keloid tissues. LINC00937 overexpression in keloid fibroblasts could repress the extracellular matrix (ECM) deposition and cell proliferation and promote MC1R expression. Moreover, high expression of miR-28-5p and low expression of LINC00937 were detected in keloid fibroblasts. We further showed that LINC00937 promoted MC1R expression by sponging miR-28-5p. Finally, our data indicated that LINC00937 inhibited the ECM deposition and proliferation of keloid fibroblasts by inhibiting miR-28-5p and facilitating MC1R expression. Overall, LINC00937 suppressed the ECM deposition and proliferation of keloid fibroblasts by acting as an miR-28-5p sponge and promoting MC1R expression. Our data suggested that LINC00937 is a potential target for keloid treatment.
- PublicationOpen AccessThe kidnapping of mitochondrial function associated with the SARS-CoV-2 infection(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Soria-Castro, Elizabeth; Soto, María Elena; Guarner-Lans, Verónica; Rojas, Gustavo; Perezpeña-Diazconti, Mario; Críales-Vera, Sergio A; Manzano Pech, Linaloe; Pérez-Torres, IsraelInfection by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) leads to multiorgan failure associated with a cytokine storm and septic shock. The virus evades the mitochondrial production of interferons through its N protein and, from that moment on, it hijacks the functions of these organelles. The aim of this study was to show how the virus kidnaps the mitochondrial machinery for its benefit and survival, leading to alterations of serum parameters and to nitrosative stress (NSS). In a prospective cohort of 15 postmortem patients who died from COVID-19, six markers of mitochondrial function (COX II, COX IV, MnSOD, nitrotyrosine, Bcl-2 and caspase-9) were analyzed by the immune colloidal gold technique in samples from the lung, heart, and liver. Biometric laboratory results from these patients showed alterations in hemoglobin, platelets, creatinine, urea nitrogen, glucose, C-reactive protein, albumin, D-dimer, ferritin, fibrinogen, Ca2+, K+, lactate and troponin. These changes were associated with alterations in the mitochondrial structure and function. The multi-organ dysfunction present in COVID-19 patients may be caused, in part, by damage to the mitochondria that results in an inflammatory state that contributes to NSS, which activates the sepsis cascade and results in increased mortality in COVID-19 patients.
- PublicationOpen AccessTraditional Chinese medicine Yiqi Huoxue recipe attenuates hepatic fibrosis via YAP/TAZ signaling(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Zhao, Wen; Zhang, Xiaoxiao; Hou, Mengmeng; Zhang, Yuguo; Tang, Yuhui; Li, Lu; Dong, Shiming; Liu, Lingdi; Zhao, Dandan; Li, Wencong; Nan, YueminBackground/Aims. The Yiqi Huoxue (YQHX) recipe has been shown to attenuate liver fibrosis, but precise mechanisms have not yet been elucidated. Recently, Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) signaling has been implicated in liver fibrogenesis. This study investigated whether the YAP/TAZ signaling is involved in the therapeutic effect of YQHX on hepatic fibrosis. Materials and Methods. Wistar rats were used to generate a model of carbon tetrachloride (CCl 4)-induced liver fibrosis. Chronic hepatitis B (CHB) patients with liver fibrosis were enrolled and assigned to receive either nucleoside/nucleotide analogues (NAs) or NAs plus YQHX. Histology, immunohistochemistry, qRT-PCR, and western blotting were conducted to mechanistically assess the therapeutic effects of YQHX on liver fibrosis. Results. YQHX markedly alleviated morphological alterations in CCl 4-induced liver fibrosis and decreased markers of hepatic fibrosis in rats. Furthermore, YQHX significantly suppressed CCl 4-meidated activation of the transforming growth factor-beta (TGF-β)/Smad signaling pathway. Notably, CCl 4 induced up-regulation of YAP, TAZ, and connective tissue growth factor (CTGF), which were significantly abrogated by YQHX. Consistent with the above major findings in rats, CHB patients treated with NAs plus YQHX had greater improvement in liver fibrosis than those given NAs alone (71.4% vs. 28.6%; P=0.057). In addition, hepatic and plasma levels of YAP were significantly decreased after YQHX treatment in CHB patients with liver fibrosis. Conclusion. YAP/TAZ signaling plays a role, at least in part, in the anti-fibrotic activity of YQHX. The findings may help to better understand the mechanisms of YQHX in the treatment of liver fibrosis
- PublicationOpen AccessExpressions of CXCL12, CXCL10 and CCL18 in Warthin tumors characterized pathologically by having a lymphoid stroma with germinal centers(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Mochizuki, Kunio; Oishi, Naoki; Masataka Kawai, Masataka Kawai; Odate, Toru; Tahara, Ippei; Kasai, Kazunari; Kondo, TetsuoThe Warthin tumor is a benign neoplasm of the salivary glands, histologically, the tumor has an oncocytic epithelial component forming uniform rows of cells surrounded by cystic spaces associated with a lymphoid stroma often showing the presence of germinal centers. The lymphoid stroma is a representative microscopic finding. If this lymphocytic accumulation is active, some sort of transmitter should exist between the Warthin tumor cells and lymphocytes. C-X-C motif chemokine ligand (CXCL) 12, CXCL10 and C-C motif chemokine ligand 18 (CCL18) are a chemoattractant for lymphocytes in vivo. There is no report on the relationship between these chemokines and Warthin tumors. In this study, we investigated these chemokines expressions in 20 Warthin tumors using immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR). For comparison, we also enrolled samples of pleomorphic adenoma, which is another benign salivary gland tumor type without prominent lymphocytic infiltration. All Warthin tumors were immunopositive for CXCL12 and CXCL10, and these reactivities were diffuse. Meanwhile, the majority of pleomorphic adenomas were immunonegative for CXCL12 (95%), CXCL10 (80%) and CCL18 (85%). Warthin tumor and pleomorphic adenoma cases were significantly different in these immunostaining expressions (CXCL12, p<0.001; CXCL10, p<0.001; CCL18, p=0.024). We examined CXCL12, CXCL10 and CCL18 mRNA expressions of 3 representative Warthin tumor samples, each having these chemokines immunopositive areas detected by RT-PCR. Finding CXCL12 and CXCL10 expressions indicate that these chemokines may play a part in the formation of a lymphoid stroma within Warthin tumors. In regards to this phenomenon, the participation of CCL18 might be restrictive compared to CXCL12 and CXCL10.