On the differentiation and origin of myoid cells in the avian thymus

1990 ◽  
Vol 181 (3) ◽  
Author(s):  
R. Seifert ◽  
B. Christ
Keyword(s):  
Myoid Cells ◽  
Avian Thymus

scholarly journals TCF21+ mesenchymal cells contribute to testis somatic cell development, homeostasis, and regeneration in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yu-chi Shen ◽  
Adrienne Niederriter Shami ◽  
Lindsay Moritz ◽  
Hailey Larose ◽  
Gabriel L. Manske ◽  
...  
Keyword(s):  
Tissue Homeostasis ◽  
Testicular Development ◽  
Myoid Cells ◽  
Regenerative Capacity ◽  
Adult Testis ◽  
Mesenchymal Progenitors ◽  
And Function ◽  
Potential Reserve ◽  
Resident Fibroblast

AbstractTesticular development and function rely on interactions between somatic cells and the germline, but similar to other organs, regenerative capacity declines in aging and disease. Whether the adult testis maintains a reserve progenitor population remains uncertain. Here, we characterize a recently identified mouse testis interstitial population expressing the transcription factor Tcf21. We found that TCF21lin cells are bipotential somatic progenitors present in fetal testis and ovary, maintain adult testis homeostasis during aging, and act as potential reserve somatic progenitors following injury. In vitro, TCF21lin cells are multipotent mesenchymal progenitors which form multiple somatic lineages including Leydig and myoid cells. Additionally, TCF21+ cells resemble resident fibroblast populations reported in other organs having roles in tissue homeostasis, fibrosis, and regeneration. Our findings reveal that the testis, like other organs, maintains multipotent mesenchymal progenitors that can be potentially leveraged in development of future therapies for hypoandrogenism and/or infertility.

scholarly journals Novel Gene Regulation in Normal and Abnormal Spermatogenesis

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 666
Author(s):  
Li Du ◽  
Wei Chen ◽  
Zixin Cheng ◽  
Si Wu ◽  
Jian He ◽  
...  
Keyword(s):  
Gene Regulation ◽  
Leydig Cells ◽  
Molecular Mechanisms ◽  
New Technologies ◽  
Genetic Regulation ◽  
Myoid Cells ◽  
Epigenetic Factors ◽  
Future Directions ◽  
New Genes ◽  
Human Spermatogenesis

Spermatogenesis is a complex and dynamic process which is precisely controlledby genetic and epigenetic factors. With the development of new technologies (e.g., single-cell RNA sequencing), increasingly more regulatory genes related to spermatogenesis have been identified. In this review, we address the roles and mechanisms of novel genes in regulating the normal and abnormal spermatogenesis. Specifically, we discussed the functions and signaling pathways of key new genes in mediating the proliferation, differentiation, and apoptosis of rodent and human spermatogonial stem cells (SSCs), as well as in controlling the meiosis of spermatocytes and other germ cells. Additionally, we summarized the gene regulation in the abnormal testicular microenvironment or the niche by Sertoli cells, peritubular myoid cells, and Leydig cells. Finally, we pointed out the future directions for investigating the molecular mechanisms underlying human spermatogenesis. This review could offer novel insights into genetic regulation in the normal and abnormal spermatogenesis, and it provides new molecular targets for gene therapy of male infertility.

scholarly journals Stromal cells from human long-term marrow cultures are mesenchymal cells that differentiate following a vascular smooth muscle differentiation pathway

Blood ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 66-76 ◽  
Author(s):  
MC Galmiche ◽  
VE Koteliansky ◽  
J Briere ◽  
P Herve ◽  
P Charbord
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Stromal Cells ◽  
Muscle Cells ◽  
Mesenchymal Cells ◽  
Myoid Cells ◽  
Marrow Cultures

In human long-term marrow cultures connective tissue-forming stromal cells are an essential cellular component of the adherent layer where granulomonocytic progenitors are generated from week 2 onward. We have previously found that most stromal cells in confluent cultures were stained by monoclonal antibodies directed against smooth muscle- specific actin isoforms. The present study was carried out to evaluate the time course of alpha-SM-positive stromal cells and to search for other cytoskeletal proteins specific for smooth muscle cells. It was found that the expression of alpha-SM in stromal cells was time dependent. Most of the adherent spindle-shaped, vimentin-positive stromal cells observed during the first 2 weeks of culture were alpha- SM negative. On the contrary, from week 3 to week 7, most interdigitated stromal cells contained stress fibers whose backbone was made of alpha-SM-positive microfilaments. In addition, in confluent cultures, other proteins specific for smooth muscle were detected: metavinculin, h-caldesmon, smooth muscle myosin heavy chains, and calponin. This study confirms the similarity between stromal cells and smooth muscle cells. Moreover, our results reveal that cells in vivo with the phenotype closest to that of stromal cells are immature fetal smooth muscle cells and subendothelial intimal smooth muscle cells; a cell subset with limited development following birth but extensively recruited in atherosclerotic lesions. Stromal cells very probably derive from mesenchymal cells that differentiate along this distinctive vascular smooth muscle cell pathway. In humans, this differentiation seems crucial for the maintenance of granulomonopoiesis. These in vitro studies were completed by examination of trephine bone marrow biopsies from adults without hematologic abnormalities. These studies revealed the presence of alpha-SM-positive cells at diverse locations: vascular smooth muscle cells in the media of arteries and arterioles, pericytes lining capillaries, myoid cells lining sinuses at the abluminal side of endothelial cells or found within the hematopoietic logettes, and endosteal cells lining bone trabeculae. More or less mature cells of the granulocytic series were in intimate contact with the thin cytoplasmic extensions of myoid cells. Myoid cells may be the in vivo counterpart of stromal cells with the above-described vascular smooth muscle phenotype.

Distribution of isoforms of the myofibrillar proteins in myoid cells of thymus

1986 ◽  
Vol 7 (4) ◽  
pp. 351-360 ◽  
Author(s):  
G. K. Dhoot ◽  
I. Dransfield ◽  
R. J. A. Grand ◽  
S. V. Perry
Keyword(s):  
Myofibrillar Proteins ◽  
Myoid Cells

scholarly journals Adrenomedullin Inhibits the Contraction of Cultured Rat Testicular Peritubular Myoid Cells Induced by Endothelin-11

2001 ◽  
Vol 64 (2) ◽  
pp. 619-624 ◽  
Author(s):  
Vittorio Santiemma ◽  
Fabio Rossi ◽  
Lara Guerrini ◽  
Athina Markouizou ◽  
Giuseppe Pasimeni ◽  
...  
Keyword(s):  
Myoid Cells

scholarly journals Regulation of GDNF expression in Sertoli cells

Reproduction ◽  
2019 ◽  
Author(s):  
Parag Parekh ◽  
Thomas Xavier Garcia ◽  
Marie-claude Hofmann
Keyword(s):  
Germ Cell ◽  
Sertoli Cells ◽  
Seminiferous Tubules ◽  
Receptor Complex ◽  
Myoid Cells ◽  
Self Renewal ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Direct Cell ◽  
Ability To Drive

Sertoli cells regulate male germ cell proliferation and differentiation and are a critical component of the spermatogonial stem cell (SSC) niche, where homeostasis is maintained by the interplay of several signaling pathways and growth factors. These factors are secreted by Sertoli cells located within the seminiferous epithelium, and by interstitial cells residing between the seminiferous tubules. Sertoli cells and peritubular myoid cells produce glial cell line-derived neurotrophic factor (GDNF), which binds to the RET/GFRA1 receptor complex at the surface of undifferentiated spermatogonia. GDNF is known for its ability to drive SSC self-renewal and proliferation of their direct cell progeny. Even though the effects of GDNF are well studied, our understanding of the regulation its expression is still limited. The purpose of this review is to discuss how GDNF expression in Sertoli cells is modulated within the niche, and how these mechanisms impact germ cell homeostasis.

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