Testicular Macrophages Produce Progesterone De Novo Promoted by cAMP and Inhibited by M1 Polarization Inducers.
Testicular Macrophages Produce Progesterone De Novo Promoted by cAMP and Inhibited by M1 Polarization Inducers.
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DOI：
10.3390/biomedicines10020487
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发表时间：
2022-02-18
期刊：
影响因子：
4.7
通讯作者：
Ogawa K
中科院分区：
文献类型：
--
作者：
Yamauchi S;Yamamoto K;Ogawa K
起源于胎儿前体的组织驻留巨噬细胞（MPEG4）通过在组织/器官特异性微环境下的自我更新来维持。在此，我们建立了一种睾丸组织驻留型睾丸间质细胞与间质细胞混合原代培养的方法。我们使用流式细胞术检查了繁殖的睾丸Møs中Møs/单核细胞标记物的表达;通过RT-PCR检测了混合培养繁殖的睾丸Møs和间质细胞中涉及睾酮产生和精子发生的基因表达;以及用环磷酸腺苷、异丙肾上腺素和M1极化诱导剂处理的繁殖睾丸Møs中孕酮（P4）的从头产生。在繁殖的MCLs中MCLs标记物表达模式与具有CD 206阳性/主要组织相容性复合体（MHC）II阴性M2表型的睾丸间质MCLs中的MCLs标记物表达模式相同。我们鉴定了参与P4产生的基因、类固醇生成所必需的转录因子和雄激素受体，并表明在M1中，P4从头产生被环磷酸腺苷和β2-肾上腺素能刺激上调，而被M1极化刺激下调。我们还证明了间质细胞和间质细胞之间缝隙连接的形成。这是第一项研究，以证明从头P4生产的组织驻留的脑膜炎。基于以往的研究揭示抑制睾酮生产的P4，我们提出，间质细胞和相邻的间质细胞之间的局部反馈机制调节睾酮的生产。这项研究中提出的结果可以促进未来的研究免疫内分泌相互作用的性腺，与不孕症和激素紊乱。
Tissue-resident macrophages (Mø) originating from fetal precursors are maintained via self-renewal under tissue-/organ-specific microenvironments. Herein, we developed a propagation method of testicular tissue-resident Mø in mixed primary culture with interstitial cells composed of Leydig cells from the mouse testis. We examined Mø/monocyte marker expression in propagated testicular Mø using flow cytometry; gene expression involved in testosterone production as well as spermatogenesis in testicular Mø and interstitial cells propagated by mixed culture via RT-PCR; and progesterone (P4) de novo production in propagated testicular Mø treated with cyclic adenosine monophosphate, isoproterenol, and M1 polarization inducers using ELISA. Mø marker expression patterns in the propagated Mø were identical to those in testicular interstitial Mø with a CD206-positive/major histocompatibility complex (MHC) II-negative M2 phenotype. We identified the genes involved in P4 production, transcription factors essential for steroidogenesis, and androgen receptors, and showed that P4 production de novo was upregulated by cyclic adenosine monophosphate and β2-adrenergic stimulation and was downregulated by M1 polarization stimulation in Mø. We also demonstrated the formation of gap junctions between Leydig cells and interstitial Mø. This is the first study to demonstrate de novo P4 production in tissue-resident Mø. Based on previous studies revealing inhibition of testosterone production by P4, we propose that local feedback machinery between Leydig cells and adjacent interstitial Mø regulates testosterone production. The results presented in this study can facilitate future studies on immune-endocrine interactions in gonads that are related to infertility and hormonal disorders.
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影响因子：
4.8
作者：
Gajardo-Gómez R;Labra VC;Orellana JA
通讯作者：
Orellana JA
影响因子：
8.8
作者：
DeFalco T;Potter SJ;Williams AV;Waller B;Kan MJ;Capel B
通讯作者：
Capel B
影响因子：
56.9
作者：
Chakarov, Svetoslav;Lim, Hwee Ying;Ginhoux, Florent
通讯作者：
Ginhoux, Florent
影响因子：
4.5
作者：
Lue, Yanhe;Wang, Christina;Swerdloff, Ronald S.
通讯作者：
Swerdloff, Ronald S.
DOI：
10.4049/jimmunol.1800352
发表时间：
2018-11-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Becerra-Díaz M;Strickland AB;Keselman A;Heller NM
通讯作者：
Heller NM