Transcriptome Analysis of the Chicken Follicular Theca Cells with miR-135a-5p Suppressed

As a class of transcription regulators, numerous miRNAs have been verified to participate in regulating ovary follicular development in chickens (Gallus gallus). Previously we showed that gga-miR-135a-5p has significant differential expression between high and low-yield chicken ovaries, and the abundance of gga-miR-135a-5p is significantly higher in follicular theca cells than in granulosa cells. However, the exact role of gga-miR-135a-5p in chicken follicular theca cells is unclear. In this study, primary chicken follicular theca cells were isolated and then transfected with gga-miR-135a-5p inhibitor. Transcriptome sequencing was performed in chicken follicular theca cells with or without transfection. Differentially expressed genes (DEGs) were analyzed using bioinformatics. A dual-luciferase reporter assay was used to verify the target relationship between gga-miR-135a-5p and predicted targets within the DEGs. Compared with the normal chicken follicle theca cells, 953 up-regulated and 1060 down-regulated genes were detected in cells with gga-miR-135a-5p inhibited. The up-regulated genes were significantly enriched in Gene Ontology terms and pathways involved in cell proliferation and differentiation. In chicken follicular theca cells, Krüppel-like factor 4 (KLF4), ATPase phospholipid transporting 8A1 (ATP8A1), and Complexin-1 (CPLX1) were significantly up-regulated when the expression of gga-miR-135a-5p was inhibited. In addition, KLF4, ATP8A1, and CPLX1 confirmed as targets of gga-miR-135a-5p by using a dual-luciferase assay in vitro. The results suggest that gga-mir-135a-5p may involve in proliferation and differentiation in chicken ovarian follicular theca cells by targeting KLF4, ATP8A1, and CPLX1.

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Critical role of integrin CD11c in splenic dendritic cell capture of missing-self CD47 cells to induce adaptive immunity

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1805542115 ◽

2018 ◽

Vol 115 (26) ◽

pp. 6786-6791 ◽

Cited By ~ 15

Author(s):

Jiaxi Wu ◽

Huaizhu Wu ◽

Jinping An ◽

Christie M. Ballantyne ◽

Jason G. Cyster

Keyword(s):

Critical Role ◽

T Cell Proliferation ◽

Cell Capture ◽

Antigen Uptake ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation ◽

Missing Self

CD11c, also known as integrin alpha X, is the most widely used defining marker for dendritic cells (DCs). CD11c can bind complement iC3b and mediate phagocytosis in vitro, for which it is also referred to as complement receptor 4. However, the functions of this prominent marker protein in DCs, especially in vivo, remain poorly defined. Here, in the process of studying DC activation and immune responses induced by cells lacking self-CD47, we found that DC capture of CD47-deficient cells and DC activation was dependent on the integrin-signaling adaptor Talin1. Specifically, CD11c and its partner Itgb2 were required for DC capture of CD47-deficient cells. CD11b was not necessary for this process but could partially compensate in the absence of CD11c. Mice with DCs lacking Talin1, Itgb2, or CD11c were defective in supporting T-cell proliferation and differentiation induced by CD47-deficient cell associated antigen. These findings establish a critical role for CD11c in DC antigen uptake and activation in vivo. They may also contribute to understanding the functional mechanism of CD47-blockade therapies.

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PI3K/PTEN/Akt and TSC/mTOR signaling pathways, ovarian dysfunction, and infertility: an update

Journal of Molecular Endocrinology ◽

10.1530/jme-14-0220 ◽

2014 ◽

Vol 53 (3) ◽

pp. R103-R118 ◽

Cited By ~ 83

Author(s):

Annu Makker ◽

Madhu Mati Goel ◽

Abbas Ali Mahdi

Keyword(s):

Signaling Pathways ◽

Ovarian Function ◽

Follicular Development ◽

Mtor Signaling ◽

Ovarian Dysfunction ◽

Primordial Follicles ◽

Current State ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation

Abnormalities in ovarian function, including defective oogenesis and folliculogenesis, represent a key female reproductive deficiency. Accumulating evidence in the literature has shown that the PI3K/PTEN/Akt and TSC/mTOR signaling pathways are critical regulators of ovarian function including quiescence, activation, and survival of primordial follicles, granulosa cell proliferation and differentiation, and meiotic maturation of oocytes. Dysregulation of these signaling pathways may contribute to infertility caused by impaired follicular development, intrafollicular oocyte development, and ovulation. This article reviews the current state of knowledge of the functional role of the PI3K/PTEN/Akt and TSC/mTOR pathways during mammalian oogenesis and folliculogenesis and their association with female infertility.

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Cell-intrinsic requirement for pRb in erythropoiesis

Blood ◽

10.1182/blood-2004-02-0618 ◽

2004 ◽

Vol 104 (5) ◽

pp. 1324-1326 ◽

Cited By ~ 42

Author(s):

Allison J. Clark ◽

Kathryn M. Doyle ◽

Patrick O. Humbert

Keyword(s):

Erythroid Differentiation ◽

Published Data ◽

Erythroid Cells ◽

Cell Cycle Exit ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation ◽

A Cell ◽

Rb Gene

Abstract Retinoblastoma (Rb) and family members have been implicated as key regulators of cell proliferation and differentiation. In particular, accumulated data have suggested that the Rb gene product pRb is an important controller of erythroid differentiation. However, current published data are conflicting as to whether the role of pRb in erythroid cells is cell intrinsic or non–cell intrinsic. Here, we have made use of an in vitro erythroid differentiation culture system to determine the cell-intrinsic requirement for pRb in erythroid differentiation. We demonstrate that the loss of pRb function in primary differentiating erythroid cells results in impaired cell cycle exit and terminal differentiation. Furthermore, we have used coculture experiments to establish that this requirement is cell intrinsic. Together, these data unequivocally demonstrate that pRb is required in a cell-intrinsic manner for erythroid differentiation and provide clarification as to its role in erythropoiesis.

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The role of IGF1 on the differentiation of prolactin secreting cells in the mouse anterior pituitary

Journal of Endocrinology ◽

10.1677/joe-09-0232 ◽

2009 ◽

Vol 203 (2) ◽

pp. 231-240 ◽

Cited By ~ 13

Author(s):

Tamiki Hikake ◽

Shinji Hayashi ◽

Taisen Iguchi ◽

Tomomi Sato

Keyword(s):

Cell Proliferation ◽

Progenitor Cells ◽

Anterior Pituitary ◽

Cell Number ◽

Postnatal Period ◽

Gh Cells ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation

IGF1 knockout (IGF1KO) mice show a reduced number of prolactin (PRL) producing cells (PRL cells); however, the role of IGF1 in PRL cell proliferation and differentiation in immature mice is unclear. In this study, ontogenic changes in the percentages of PRL cells, GH producing cells (GH cells), and 5-bromo-2′-deoxyuridine (BrdU)-labeled cells in the anterior pituitary of male IGF1KO mice during the postnatal period were investigated. The percentage of PRL cells in IGF1KO mice was significantly lower at day 20 compared with that in wild-type (WT) mice, while GH cells in IGF1KO mice were significantly increased from day 10. From days 5 to 20, the percentage of BrdU-labeled cells in WT and IGF1KO mice was similar. PRL cells and GH cells are thought to originate from the same progenitor cells, therefore, PRL cells in IGF1KO mice are not able to differentiate because progenitor cells have already committed to be GH cells. However, IGF1, 17β-estradiol (E2), epidermal growth factor (EGF), or IGF1 plus E2 treatments increased the PRL cell number in the pituitaries in vitro of 10-day-old WT and IGF1KO mice. This fact suggests that these factors are involved in PRL cell proliferation and differentiation. In addition, the increase of PRL cells in IGF1KO mice stimulated by E2 or EGF was less than that of WT mice. Thus, IGF1 plays a crucial role in PRL cell proliferation and differentiation in mouse pituitaries by regulating the differentiation of progenitor cells and mediating the actions of E2 and EGF.

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The role of progesterone in regulating human granulosa cell proliferation and differentiation in vitro.

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jcem.76.3.8445028 ◽

1993 ◽

Vol 76 (3) ◽

pp. 696-700

Author(s):

L M Chaffkin ◽

A A Luciano ◽

J J Peluso

Keyword(s):

Cell Proliferation ◽

Granulosa Cell ◽

Human Granulosa Cell ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation

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Targeting cholesterol homeostasis in hematopoietic malignancies

Blood ◽

10.1182/blood.2021012788 ◽

2021 ◽

Author(s):

Andrea Brendolan ◽

Vincenzo Russo

Keyword(s):

Cholesterol Homeostasis ◽

Cell Integrity ◽

Cellular Functions ◽

Hematopoietic Malignancies ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation ◽

X Receptors

Cholesterol is a vital lipid for cellular functions. It is necessary for membrane biogenesis, cell proliferation and differentiation. In addition to maintaining cell integrity and permeability, increasing evidence indicates a strict link between cholesterol homeostasis, inflammation and haematological tumors. This makes cholesterol homeostasis an optimal therapeutic target for hematopoietic malignancies. Manipulating cholesterol homeostasis either interfering with its synthesis or activating the reverse cholesterol transport via the engagement of liver X receptors (LXRs), affects the integrity of tumor cells both in vitro and in vivo. Cholesterol homeostasis has also been manipulated to restore antitumor immune responses in preclinical models. These observations have prompted clinical trials in acute myeloid leukemia (AML) to test the combination of chemotherapy with drugs interfering with cholesterol synthesis, i.e. statins. We review the role of cholesterol homeostasis in hematopoietic malignancies, as well as in cells of the tumor microenvironment, and discuss the potential use of lipid modulators for therapeutic purposes.

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004.Control of skeletal muscle cell proliferation and differentiation

Reproduction Fertility and Development ◽

10.1071/srb05abs004 ◽

2005 ◽

Vol 17 (9) ◽

pp. 63

Author(s):

M. Grounds

Keyword(s):

Skeletal Muscle ◽

Cell Proliferation ◽

Multinucleated Cells ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation ◽

The Matrix ◽

Key Issues

Skeletal muscle is formed by mononucleated precursor cells (myoblasts) that cease cell proliferation to start differentiation; this results in fusion between the myoblasts to form multinucleated cells (myotubes) that continue to differentiate (and fuse with more muscle cells) and mature into myofibres. Myogenesis has been widely used as a model to study in vitro factors controlling cell proliferation and differentiation. Condition in vitro may not reflect what happens in the more complex in vivo environment. Some of the key issues are what activates quiescent myoblasts in mature skeletal muscle in vivo, and what controls the switch between proliferation and differentiation? The role of the matrix, and molecules such as MyoD, p53, NFAT and IGF-1 will be considered.

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Targeting of SET/I2PP2A oncoprotein inhibits Gli1 transcription revealing a new modulator of Hedgehog signaling

Scientific Reports ◽

10.1038/s41598-021-93440-0 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Iliana Serifi ◽

Simoni Besta ◽

Zoe Karetsou ◽

Panagiota Giardoglou ◽

Dimitris Beis ◽

...

Keyword(s):

Mammalian Cells ◽

Hedgehog Signaling ◽

Luciferase Reporter ◽

Loss Of Function ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation ◽

Patterning Defect ◽

Hh Signaling ◽

Expression In Mammalian Cells

AbstractThe Hedgehog (Hh)/Gli signaling pathway controls cell proliferation and differentiation, is critical for the development of nearly every tissue and organ in vertebrates and is also involved in tumorigenesis. In this study, we characterize the oncoprotein SET/I2PP2A as a novel regulator of Hh signaling. Our previous work has shown that the zebrafish homologs of SET are expressed during early development and localized in the ciliated organs. In the present work, we show that CRISPR/Cas9-mediated knockdown of setb gene in zebrafish embryos resulted in cyclopia, a characteristic patterning defect previously reported in Hh mutants. Consistent with these findings, targeting setb gene using CRISPR/Cas9 or a setb morpholino, reduced Gli1-dependent mCherry expression in the Hedgehog reporter zebrafish line Tg(12xGliBS:mCherry-NLS). Likewise, SET loss of function by means of pharmacological inhibition and gene knockdown prevented the increase of Gli1 expression in mammalian cells in vitro. Conversely, overexpression of SET resulted in an increase of the expression of a Gli-dependent luciferase reporter, an effect likely attributable to the relief of the Sufu-mediated inhibition of Gli1. Collectively, our data support the involvement of SET in Gli1-mediated transcription and suggest the oncoprotein SET/I2PP2A as a new modulator of Hedgehog signaling.

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