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

2009 ◽  
Vol 203 (2) ◽  
pp. 231-240 ◽  
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.

004.Control of skeletal muscle cell proliferation and differentiation

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.

scholarly journals Potential role of marine algae extract on 3T3-L1 cell proliferation and differentiation: an in vitro approach

2016 ◽  
Vol 49 (1) ◽  
Author(s):  
Soundharrajan Ilavenil ◽  
Da Hye Kim ◽  
Mayakrishnan Vijayakumar ◽  
Srisesharam Srigopalram ◽  
Sang Gun Roh ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Marine Algae ◽  
Potential Role ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

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

2018 ◽  
Vol 115 (26) ◽  
pp. 6786-6791 ◽  
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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