Unexpected requirement for a binding partner of the syntaxin family in phagocytosis by murine testicular Sertoli cells

Ys, Dong; Hou, W.; Y, Li; Db, Liu; Gz, Hao; Hf, Zhang; Jc, Li; Zhao, Jie; Zhang, S; Gb, Liang; Li, Wei

doi:10.1038/cdd.2015.139

Cited by 74 publications

(55 citation statements)

References 54 publications

(67 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Besides, the presence of serum influences phagocytic activity and may inhibit the response to certain hormones such as FSH (Monaco, Adamo, Stefanini, & Conti, 1989;Xiong et al, 2008). Sertoli cells retain their viability, morphology, and secretory activity in the absence of serum (Skinner & Griswold, 1982); however, most reports describe the use of normal serum conditions for Sertoli primary cultures without negative consequences (Ahmadi et al, 2018;Dong et al, 2016;Doyle et al, 2012). Although the starvation method may be a promising strategy to achieve purer Sertoli cell populations, a comparative study on the effect of different serum conditions should be undertaken to further elucidate its efficacy.…”

Section: Methods To Isolate Rodent Sertoli Cellsmentioning

confidence: 99%

Characterization of rodent Sertoli cell primary cultures

Zomer

Reddi

2020

Molecular Reproduction Devel

View full text Add to dashboard Cite

Sertoli cells play a vital role in spermatogenesis by offering physical and nutritional support to the differentiating male germ cells. They form the blood–testis barrier and secrete growth factors essential for germ cell differentiation. Sertoli cell primary cultures are critical for understanding the regulation of spermatogenesis; however, obtaining pure cultures has been a challenge. Rodent Sertoli cell isolation protocols do not rule out contamination by the interstitial or connective tissue cells. Sertoli cell‐specific markers could be helpful, but there is no consensus. Vimentin, the most commonly used marker, is not specific for Sertoli cells since its expression has been reported in peritubular myoid cells, mesenchymal stem cells, fibroblasts, macrophages, and endothelial cells, which contaminate Sertoli cell preparations. Markers based on transcription and growth factors also have limitations. Thus, the impediment to obtaining pure Sertoli cell cultures pertains to both the method of isolation and marker usage. The aim of this review is to discuss improvements to current methods of rodent Sertoli cell primary cultures, assess the properties of prepubertal versus mature Sertoli cell cultures, and propose steps to improve cellular characterization. Potential benefits of using contemporary approaches, including lineage tracing, specific cell ablation, and RNA‐seq for obtaining Sertoli‐specific transcript markers are discussed. Evaluating the specificity and applicability of these markers at the protein level to characterize Sertoli cells in culture would be critical. This review is expected to positively impact future work using primary cultures of rodent Sertoli cells.

show abstract

Section: Methods To Isolate Rodent Sertoli Cellsmentioning

confidence: 99%

Characterization of rodent Sertoli cell primary cultures

Zomer

Reddi

2020

Molecular Reproduction Devel

View full text Add to dashboard Cite

show abstract

“…Total RNA isolation and cDNA synthesis were carried out according to an established protocol . The strength of expression of different genes was determined by a Qiagen (Shanghai, China) protocol using an ABI Prism 7300 instrument and SYBR Green reagents (Applied Biosystems, Foster City, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Synovial GATA1 mediates rheumatoid arthritis progression via transcriptional activation of NOS2 signaling

Liu¹,

Wei²,

Zhi³

et al. 2018

Microbiology and Immunology

View full text Add to dashboard Cite

Transcriptional regulation of inducible nitric oxide synthase (iNOS) is critically involved in the pathogenesis and progression of rheumatoid arthritis (RA); however, the specific transcription factors that control this process remain largely unidentified. In the present study, it was discovered that expression of the key erythroid factor, globin transcription factor 1 (GATA1), is significantly greater in human RA synovial tissues than in osteoarthritis (OA) tissues. IL 6 was found to induce synovial GATA1 expression in a signal transducer and activator of transcription 3-dependent manner. Functionally, knockdown of GATA1 expression using specific small interfering RNA treatment was found to compromise immunoreaction-elicited expression of proinflammatory cytokines and thus impair invasiveness of the human fibroblast-like synovial cell line MH7A, whereas introduction of exogenous GATA1 was found to promote production of proinflammatory cytokines, leading to greater aggressiveness of MH7A cells. Mechanistically, GATA1 acts as the transcriptional coactivator of NOS2 (the gene encoding iNOS) transcription. Collectively, these data suggest that synovial GATA1 is an essential contributor to development and exacerbation of RA, presumably by inducing NOS2 transcription.

show abstract

“…Total RNA extraction, reverse transcription and PCR were carried out as described previously (Dong et al 2016). Routine DNase (Applied Biosystems/Ambion) treatment (1 unit of DNase I/μg of total RNA) was performed before RT.…”

Section: Rt-qpcrmentioning

confidence: 99%

KLF14 potentiates oxidative adaptation via modulating HO-1 signaling in castrate-resistant prostate cancer

Luo

Liu

Wang

et al. 2019

Endocrine-Related Cancer

View full text Add to dashboard Cite

Insights into the mechanisms by which key factors stimulate cell growth under androgen-depleted conditions is a premise to the development of effective treatments with clinically significant activity in patients with castration-resistant prostate cancer (CRPC). Herein, we report that, the expression of Krüppel-like factor 14 (KLF14), a master transcription factor in the regulation of lipid metabolism, was significantly induced in castration-insensitive PCa cells and tumor tissues from a mouse xenograft model of CRPC. KLF14 upregulation in PCa cells, which was stimulated upstream by oxidative stress, was dependent on multiple pathways including PI3K/AKT, p42/p44 MAPK, AMPK and PKC pathways. By means of ectopic overexpression and genetic inactivation, we further show that KLF14 promoted cell growth via positive regulation of the antioxidant response under androgen-depleted conditions. Mechanistically, KLF14 coupled to p300 and CBP to enhance the transcriptional activation of HMOX1, the gene encoding the antioxidative enzyme heme oxygenase-1 (HO-1) that is one of the most important mechanisms of cell adaptation to stress. Transient knockdown of HMOX1 is sufficient to overcome KLF14 overexpression-potentiated PCa cell growth under androgen-depleted conditions. From a pharmacological standpoint, in vivo administration of ZnPPIX (a specific inhibitor of HO-1) effectively attenuates castration-resistant progression in the mouse xenograft model, without changing KLF14 level. Together, these results provide comprehensive insight into the KLF14-dependent regulation of antioxidant response and subsequent pathogenesis of castration resistance and indicate that interventions targeting the KLF14/HO-1 adaptive mechanism should be further explored for CRPC treatment.

show abstract

Unexpected requirement for a binding partner of the syntaxin family in phagocytosis by murine testicular Sertoli cells

Cited by 74 publications

References 54 publications

Characterization of rodent Sertoli cell primary cultures

Characterization of rodent Sertoli cell primary cultures

Synovial GATA1 mediates rheumatoid arthritis progression via transcriptional activation of NOS2 signaling

KLF14 potentiates oxidative adaptation via modulating HO-1 signaling in castrate-resistant prostate cancer

Contact Info

Product

Resources

About