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Kinases in bone homeostasis: Studies...

Kang, Heeseog.

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Kinases in bone homeostasis: Studies on the roles of AMPKalpha2 and PI3Kgamma in bone homeostasis.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Kinases in bone homeostasis: Studies on the roles of AMPKalpha2 and PI3Kgamma in bone homeostasis./
作者:	Kang, Heeseog.
面頁冊數:	120 p.
附註:	Source: Dissertation Abstracts International, Volume: 71-06, Section: B, page: 3446.
Contained By:	Dissertation Abstracts International71-06B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3411466
ISBN:	9781124042732

Kinases in bone homeostasis: Studies on the roles of AMPKalpha2 and PI3Kgamma in bone homeostasis.
Kang, Heeseog.

Kinases in bone homeostasis: Studies on the roles of AMPKalpha2 and PI3Kgamma in bone homeostasis. - 120 p.

Source: Dissertation Abstracts International, Volume: 71-06, Section: B, page: 3446.

Thesis (Ph.D.)--University of Connecticut, 2010.

AMPKalpha2 is a catalytic subunit of AMPK, which is a key regulator for cellular and whole body energy homeostasis. Bone is a dynamic organ and susceptible to metabolic changes. To assess the physiological role of AMPKalpha2 in bone homeostasis, we characterized bone phenotype of AMPKalpha2 KO mice. We found that AMPKalpha2 KO mice have lower bone mass than WT littermates and it was accounted for by the increased osteoclast development. The increased osteoclastogenesis of AMPKalpha2deficient macrophages in vitro was associated with the up-regulated expression of osteoclast-associated marker genes. To further elucidate how AMPKalpha2 modulates RANKL-mediated osteoclast formation, we examined global gene expression profiles of BMM-OCL via microarray analysis. Surprisingly, many of the genes that were up-regulated by AMPKalpha2 deficiency were associated with bone marrow stromal cells. Smooth muscle alpha-actin (SMAA), which was among the up-regulated genes in AMPKalpha2 KO, was utilized for our further investigation on the role of AMPKalpha2-deficient stromal cells in the increased osteoclastogenesis of AMPKalpha2-deficient BMM-OCL. Experiments with SMAA-GFP;AMPKalpha2 KO mice exhibited that the increased growth rate of AMPKalpha2-deficient stromal cells was a contributing factor for the elevated osteoclastogenesis in AMPKalpha2-deficent BMM-OCL.

ISBN: 9781124042732Subjects--Topical Terms:

1017730
Biology, Genetics.

Kinases in bone homeostasis: Studies on the roles of AMPKalpha2 and PI3Kgamma in bone homeostasis.
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500 $a Adviser: Dianqing Wu.
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520 $a AMPKalpha2 is a catalytic subunit of AMPK, which is a key regulator for cellular and whole body energy homeostasis. Bone is a dynamic organ and susceptible to metabolic changes. To assess the physiological role of AMPKalpha2 in bone homeostasis, we characterized bone phenotype of AMPKalpha2 KO mice. We found that AMPKalpha2 KO mice have lower bone mass than WT littermates and it was accounted for by the increased osteoclast development. The increased osteoclastogenesis of AMPKalpha2deficient macrophages in vitro was associated with the up-regulated expression of osteoclast-associated marker genes. To further elucidate how AMPKalpha2 modulates RANKL-mediated osteoclast formation, we examined global gene expression profiles of BMM-OCL via microarray analysis. Surprisingly, many of the genes that were up-regulated by AMPKalpha2 deficiency were associated with bone marrow stromal cells. Smooth muscle alpha-actin (SMAA), which was among the up-regulated genes in AMPKalpha2 KO, was utilized for our further investigation on the role of AMPKalpha2-deficient stromal cells in the increased osteoclastogenesis of AMPKalpha2-deficient BMM-OCL. Experiments with SMAA-GFP;AMPKalpha2 KO mice exhibited that the increased growth rate of AMPKalpha2-deficient stromal cells was a contributing factor for the elevated osteoclastogenesis in AMPKalpha2-deficent BMM-OCL.
520 $a G protein-coupled receptor-regulated PI3Kgamma is abundantly expressed in myeloid cells and became a promising drug target to treat various inflammatory diseases. However, its role in bone homeostasis has not been documented. We therefore characterized bone phenotype of PI3Kgamma-deficient mice and found that PI3Kgamma-deficient mice had higher bone mass than WT littermates. Our analyses further revealed that PI3Kgamma deficiency did not affect the bone formation because no significant changes in osteoblast number and bone formation rate were observed. Instead, the lack of PI3Kgamma was associated with decreased bone resorption as evidenced by decreased osteoclast number in vivo and impaired osteoclast formation in vitro. The decreased osteoclast formation was accompanied by down-regulated expression of osteoclastogenic genes, compromised chemokine receptor signaling, and an increase in apoptosis during osteoclast differentiation. These data suggest that PI3Kgamma regulates bone homeostasis by modulating osteoclastogenesis. Our study also suggests that inhibition of PI3Kgamma, which is being considered as a potential therapeutic strategy for treating chronic inflammatory disorders, may result in an increase in bone mass.
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