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Spermatogenesis, heat stress and male infertility
Published in Rajender Singh, Molecular Signaling in Spermatogenesis and Male Infertility, 2019
Understanding how HSF1 and HSF2 respond to temperatures in the testis has clarified both speed and downstream events of different heat stress animal and cellular models. We still need to bring together researchers examining contraception action and maximizing germ cell production/survival to understand how molecular models and events affect spermatogenesis.
Heat shock transcription factor 2 predicts mucosal healing and promotes mucosal repair of ulcerative colitis
Published in Scandinavian Journal of Gastroenterology, 2020
Yunling Wen, Junkun Niu, Fengrui Zhang, Jing Wu, Maojuan Li, Yang Sun, Wen Wang, Shuxian Xia, Ying Tan, Kunhua Wang, Yinglei Miao
In our previous research, we discovered that heat shock transcription factor 2 (HSF2) was differentially expressed in UC patients and increased in parallel with the activity of UC. Moreover, the expression of HSF2 in the intestinal mucosa of UC patients was significantly higher than that in Crohn’s disease, Behcet’s disease, intestinal tuberculosis, infective enteritis and intestinal lymphoma [14]. Furthermore, hsf2-/-mice exhibited more severe intestinal inflammation than wild-type mice in a DSS-induced colitis model [15]. These results suggest that HSF2 plays an important role in the pathogenesis of UC and appears to be a novel potential biomarker for UC assessment. HSF2 belongs to the heat shock transcription factor (HSF) family, which are DNA-binding proteins that regulate heat shock protein (HSP) transcription, playing a central role in the heat shock response. Heat shock responses are ubiquitous and exist in all organisms to protect cells against harmful conditions, including heat shock, oxidative stress and microbial infection [16]. Previous evidence has shown that HSF1 and HSP70 play roles in protecting against DSS-induced colitis [17]. HSP70 has been reported to prevent TLR4-mediated intestinal inflammation [18] and accelerate wound healing [19]. HSP27 regulates colonic myofibroblast migration and plays an important role in MH in the setting of inflammation [20]. HSP90, HSP70, and HSP27 all regulate the TGF-β/Smad signaling pathway [21–23]. The above studies indicated that HSF1 and HSPs are important for intestinal inflammation and mucosal repair in UC. Accordingly, we hypothesized that HSF2 has a similar effect, but the role of HSF2 in MH is unclear. To confirm this hypothesis, we conducted this study.