scholarly journals Human Testicular Peritubular Cells Host Putative Stem Leydig Cells With Steroidogenic Capacity

2014 ◽  
Vol 99 (7) ◽  
pp. E1227-E1235 ◽  
Author(s):  
Luise Landreh ◽  
Katrin Spinnler ◽  
Kerstin Schubert ◽  
Merja R. Häkkinen ◽  
Seppo Auriola ◽  
...  
Keyword(s):  
Growth Factor ◽  
Leydig Cell ◽  
Regulatory Protein ◽  
Cell Lineage ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Steroidogenic Acute Regulatory Protein ◽  
Rt Pcr ◽  
Steroidogenic Acute Regulatory ◽  
Peritubular Cells

Aim: We aim to examine the steroidogenic phenotype and the differentiation potential of human testicular peritubular cells (HTPCs) and to explore their possible relationship to the adult Leydig cell lineage. Background: The cells of the adult Leydig cell lineage may reside in the peritubular compartment of the testis. This suggestion is supported by the facts that the rodent peritubular cells can be differentiated toward this lineage and that cAMP enhances their steroidogenic potential. Methods: Human testicular biopsies, and derived HTPCs, were analyzed by immunohistochemistry, RT-PCR, and Western blotting. After stimulation by forskolin or platelet-derived growth factor-BB, quantitative RT-PCR was used to compare the levels of mRNAs encoding proteins involved in steroidogenesis and steroid production was analyzed by liquid chromatography and tandem mass spectrometry. Results: Immunohistochemical analysis revealed that the peritubular cells that form the outer part of the tubular wall express platelet derived growth factor receptor-α. Furthermore, the pluripotency markers (POU domain class 5 transcription factor 1, GATA-binding protein 4), stem Leydig cell markers (platelet derived growth factor receptor-A, leukemia inhibitory factor receptor), and mRNAs encoding proteins involved in steroidogenesis (nuclear receptor subfamily 5, group A, member 1; steroidogenic acute regulatory protein; CYP11A1; CYP17A1; 3β-hydroxysteroid dehydrogenase) were expressed by the HTPCs. Stimulation with forskolin increased the expression of the steroidogenic markers, which was accompanied by the production of pregnenolone and progesterone by HTPCs in vitro. Treatment with platelet-derived growth factor-BB induced expression of steroidogenic acute regulatory protein. Conclusions: Our results indicate that the tubular wall of the human testis is a reservoir for cells of the adult Leydig cell lineage and that the steroidogenic potential of these cells can be activated in culture.

scholarly journals Tumor Necrosis Factor-α Inhibits Leydig Cell Steroidogenesis through a Decrease in Steroidogenic Acute Regulatory Protein Expression1

Endocrinology ◽  
1998 ◽  
Vol 139 (6) ◽  
pp. 2863-2868 ◽  
Author(s):  
Claire Mauduit ◽  
Françoise Gasnier ◽  
Catherine Rey ◽  
Marie-Agnès Chauvin ◽  
Douglas M. Stocco ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Leydig Cell ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Regulatory Protein ◽  
Steroidogenic Acute Regulatory Protein ◽  
Steroidogenic Acute Regulatory ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Regulation by Adrenocorticotropin (ACTH), Angiotensin II, Transforming Growth Factor-β, and Insulin-Like Growth Factor I of Bovine Adrenal Cell Steroidogenic Capacity and Expression of ACTH Receptor, Steroidogenic Acute Regulatory Protein, Cytochrome P450c17, and 3β-Hydroxysteroid Dehydrogenase*

Endocrinology ◽  
2000 ◽  
Vol 141 (5) ◽  
pp. 1599-1607 ◽  
Author(s):  
Christine Le Roy ◽  
J. Yuan Li ◽  
Douglas M. Stocco ◽  
Dominique Langlois ◽  
José M. Saez
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Regulatory Protein ◽  
Hydroxysteroid Dehydrogenase ◽  
Steroidogenic Acute Regulatory Protein ◽  
Mrna Levels ◽  
Factor I ◽  
Acth Receptor ◽  
Igf I ◽  
Steroidogenic Acute Regulatory

Abstract The purpose of this study was to evaluate the time-course effect of a 36-h treatment with ACTH (10−8m), transforming growth factor-β1 (TGFβ1; 10−10m), angiotensin II (AngII; 10−7m), and insulin-like growth factor I (IGF-I; 10−8m) on the steroidogenic capacity of bovine adrenocortical cells (BAC) and on messenger RNA (mRNA) levels of ACTH receptor, cytochrome P450c17, 3β-hydroxysteroid dehydrogenase (3βHSD), steroidogenic acute regulatory protein (StAR), and StAR protein. ACTH and IGF-I enhanced, in a time-dependent manner, the acute 2-h ACTH-induced cortisol production, whereas TGFβ1 and AngII markedly reduced it. ACTH, IGF-I, and AngII increased ACTH receptor mRNA, but the opposite was observed after TGFβ1 treatment. ACTH and IGF-I increased P450c17 and 3βHSD mRNAs, whereas AngII and TGFβ1 had the opposite effects. However, the effects of the four peptides on ACTH-induced cortisol production appeared before any significant alterations of the mRNA levels occurred. The most marked and rapid effect of the four peptides was on StAR mRNA. The stimulatory effect of ACTH was seen within 1.5 h, peaked at 4–6 h, and declined thereafter, but at the end of the 36-h pretreatment, the levels of StAR mRNA and protein were higher than those in control cells. IGF-I also enhanced StAR mRNA levels within 1.5 h, and these levels remained fairly constant. The effects of AngII on StAR mRNA expression were biphasic, with a peak within 1.5–3 h, followed by a rapid decline to almost undetectable levels of both mRNA and protein. TGFβ1 had no significant effect during the first 3 h, but thereafter StAR mRNA declined, and at the end of the experiment the StAR mRNA and protein were almost undetectable. Similar results were observed when cells were treated with ACTH plus TGFβ1. A 2-h acute ACTH stimulation at the end of the 36-h pretreatment caused a higher increase in StAR mRNA and protein in ACTH- or IGF-I-pretreated cells than in control cells, which, in turn, had higher levels than cells pretreated with TGFβ1, ACTH plus TGFβ1, or AngII. These results and the fact that the stimulatory (IGF-I) or inhibitory (AngII and TGFβ1) effects on ACTH-induced cortisol production were more pronounced than those on the ability of cells to transform pregnenolone into cortisol strongly suggest that regulation of StAR expression is one of the main factors, but not the only one, involved in the positive (IGF-I) or negative (TGFβ1 and AngII) regulation of BAC for ACTH steroidogenic responsiveness. A high correlation between steady state mRNA level and acute ACTH-induced cortisol production favors this conclusion.

Characterization of the platelet-derived growth factor receptor-α-positive cell lineage during murine late lung development

2015 ◽  
Vol 309 (9) ◽  
pp. L942-L958 ◽  
Author(s):  
Aglaia Ntokou ◽  
Friederike Klein ◽  
Daria Dontireddy ◽  
Sven Becker ◽  
Saverio Bellusci ◽  
...  
Keyword(s):  
Growth Factor ◽  
Lung Development ◽  
Smooth Muscle Actin ◽  
Cell Lineage ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Adult Lung ◽  
Tip Cells

A reduced number of alveoli is the structural hallmark of diseases of the neonatal and adult lung, where alveoli either fail to develop (as in bronchopulmonary dysplasia), or are progressively destroyed (as in chronic obstructive pulmonary disease). To correct the loss of alveolar septa through therapeutic regeneration, the mechanisms of septa formation must first be understood. The present study characterized platelet-derived growth factor receptor-α-positive (PDGFRα+) cell populations during late lung development in mice. PDGFRα+ cells (detected using a PDGFRαGFP reporter line) were noted around the proximal airways during the pseudoglandular stage. In the canalicular stage, PDGFRα+ cells appeared in the more distal mesenchyme, and labeled α-smooth muscle actin-positive tip cells in the secondary crests and lipofibroblasts in the primary septa during alveolarization. Some PDGFRα+ cells appeared in the mesenchyme of the adult lung. Over the course of late lung development, PDGFRα+ cells consistently expressed collagen I, and transiently expressed markers of mesenchymal stem cells. With the use of both, a constitutive and a conditional PDGFRαCre line, it was observed that PDGFRα+ cells generated alveolar myofibroblasts including tip cells of the secondary crests, and lipofibroblasts. These lineages were committed before secondary septation. The present study provides new insights into the time-dependent commitment of the PDGFRα+ cell lineage to lipofibroblasts and myofibroblasts during late lung development that is needed to better understand the cellular contribution to the process of alveolarization.

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