Literature DB >> 30899363

Telocytes enhanced the proliferation, adhesion and motility of endometrial stromal cells as mediated by the ERK pathway in vitro.

Xue-Ling Tang1, Fei-Lei Zhang1, Xiao-Juan Jiang1, Xiao-Jun Yang1.   

Abstract

Telocytes (TCs) is special interstitial cell that have recently been identified in the female reproductive system. Endometriosis (EMs) is a benign gynecological disease whose etiology is still not fully clear. Implantation and proliferation of endometrial stromal cells (ESCs) out of the uterus are essential processes in the development of EMs. Herein, we investigate the in vitro changes of ESCs when cocultured with TCs, and the potential mechanisms involved. The current results demonstrated that, vimentin-positive/pan cytokeratin-negative ESCs, and TCs with a characteristic structure and immunophenotype (CD34/vimentin double-positive) were successfully isolated and harvested. Morphologically, direct cell-to-cell contacts were observed between TCs and ESCs. Quantitatively, TCs treatment clearly promotes the viability of ESCs, enhances cell cycle progression at G2/M phase and upregulates p-ERK1/2 and cyclin-D3 (all P < 0.05). Functionally, ESCs educated by TCs displayed significantly enhanced adhesion ability and accelerated invasion and migration capacity (all P < 0.05). However, no significant changes were found in the rate of apoptosis and in the expression of AKT signaling pathway proteins in TCs-educated ESCs (both P > 0.05). Therefore, TCs treatment obviously enhanced the in vitro motile and invasive capacity of ESCs, which were mediated by the ERK-cyclin-D3 signaling pathway, likely through direct intercellular contacts and/or juxta-paracrine effects; signaling through this axis therefore increased the likelihood of EMs. The enhanced functions of TCs-educated ESCs not only contribute to a deeper understanding of TCs, but also highlight a new concept regarding the physiopathology and therapy of EMs and associated impaired reproductive function.

Entities:  

Keywords:  EMs-related diseases; Telocytes (TCs); endometrial stromal cells (ESCs); endometriosis (EMs); extracellular-regulated kinase (ERK) signaling pathway; interstitial cells

Year:  2019        PMID: 30899363      PMCID: PMC6413249     

Source DB:  PubMed          Journal:  Am J Transl Res            Impact factor:   4.060


  6 in total

1.  The Mechanism of Wnt Pathway Regulated by Telocytes to Promote the Regeneration and Repair of Intrauterine Adhesions.

Authors:  Cai-Zhen Zhao; Ping Fu; Wen-Ying Peng; Na Pan; Yuqiu Peng; Min Zhao; Weiquan Xie
Journal:  Comput Math Methods Med       Date:  2022-07-06       Impact factor: 2.809

2.  RhoA/ROCK pathway mediates the effect of oestrogen on regulating epithelial-mesenchymal transition and proliferation in endometriosis.

Authors:  Zhi-Xiong Huang; Xiao-Mei Mao; Rong-Feng Wu; Shao-Min Huang; Xin-Yu Ding; Qiong-Hua Chen; Qing-Xi Chen
Journal:  J Cell Mol Med       Date:  2020-07-29       Impact factor: 5.310

3.  From TELOCYTES to TELOCYTOPATHIES. Do Recently Described Interstitial Cells Play a Role in Female Idiopathic Infertility?

Authors:  Martin Klein; Lenka Lapides; Denisa Fecmanova; Ivan Varga
Journal:  Medicina (Kaunas)       Date:  2020-12-11       Impact factor: 2.430

Review 4.  Telocytes in the Female Reproductive System: Up-to-Date Knowledge, Challenges and Possible Clinical Applications.

Authors:  Martin Klein; Mária Csöbönyeiová; Ľuboš Danišovič; Lenka Lapides; Ivan Varga
Journal:  Life (Basel)       Date:  2022-02-10

Review 5.  Telocytes in Fibrosis Diseases: From Current Findings to Future Clinical Perspectives.

Authors:  Xiao-Jiao Wei; Tian-Quan Chen; Xiao-Jun Yang
Journal:  Cell Transplant       Date:  2022 Jan-Dec       Impact factor: 4.139

6.  MicroRNA‑202 inhibits endometrial stromal cell migration and invasion by suppressing the K‑Ras/Raf1/MEK/ERK signaling pathway.

Authors:  Di Zhang; Ling Wang; Hua-Lei Guo; Zi-Wei Zhang; Chong Wang; Ri-Cheng Chian; Zhi-Fen Zhang
Journal:  Int J Mol Med       Date:  2020-10-09       Impact factor: 4.101

  6 in total

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