TGF-β1-induced collagen promotes chicken ovarian follicle development via an intercellular cooperative pattern.
Shuo ZhouYanfen MaJinwei YaoAn ZhaoChukang XieYuling MiCaiqiao ZhangPublished in: Cell biology international (2021)
Follicle development is a complex process under strict regulation of diverse hormones and cytokines including transforming growth factor β (TGF-β) superfamily members. TGF-β is pivotal for the regulation of ovarian functions under physiological and pathological conditions. In this study, effect of TGF-β1 on chicken follicle development was examined through investigating the accumulation and action of collagen, an indispensable member of the extracellular matrix (ECM) involved in this process. The granulosa cells (GCs) and theca cells (TCs) were separated from growing follicles of the laying chicken for treatment of TGF-β1 and analysis of expression of ECM components and key proteins in intracellular signaling pathways. Results showed that collagen was mainly distributed in the follicular theca layer and was produced with the formation of the granulosa layer during ovarian development. Collagen accumulation increased with follicle growth and treatment of GCs with TGF-β1 elicited an increased expression of collagen. After production from GCs, collagen was transferred to the neighboring TCs to promote cell proliferation and inhibit apoptosis. Treatment of collagen remarkably increased expression of p-ERK, mitogen-activated protein kinase (MAPK), and p-MAPK, but treatment with hydroxylase inhibitor (to break collagen structure) reversed these alterations. In conclusion, during follicle growth collagen was secreted by GCs under TGF-β1 stimulation and was subsequently collaboratively transferred to neighboring TCs to increase cell proliferation and thus to promote follicle development via an intercellular cooperative pattern during development of chicken growing follicles.
Keyphrases
- transforming growth factor
- cell proliferation
- wound healing
- extracellular matrix
- epithelial mesenchymal transition
- tissue engineering
- signaling pathway
- poor prognosis
- induced apoptosis
- cell cycle arrest
- oxidative stress
- pi k akt
- type diabetes
- binding protein
- endoplasmic reticulum stress
- diabetic rats
- insulin resistance
- tyrosine kinase
- high glucose
- long non coding rna
- cell adhesion