Mechanisms underlying glucocorticoid-induced osteocyte dysfunction

Junjie Gao

doi:10.4225/23/59d33d161fd5b

Mechanisms underlying glucocorticoid-induced osteocyte dysfunction

Junjie Gao

UWA Medical School

Research output: Thesis › Doctoral Thesis

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Abstract

The therapeutic functions of Glucocorticoids (GCs) are unfortunately accompanied by severe bone loss. Being the most abundant cell type in bone, osteocytes are highly susceptible to the adverse effects of GC treatment. In this thesis, the deleterious effects of GC on osteocytes and the underlying mechanisms governing these effects were explored and addressed: (1) GC regulates osteocyte-mediated bone modification and exosomal secretion; (2) GC impairs osteocyte communication by inducing autophagy-mediated degradation of Cx43; (3) GC inhibits ER-mediated mitochondrial transfer within the osteocyte processes; and (4) GC induces REDD1 to regulate autophagy via interaction with Akt-mTORC1 signalling.

Original language	English
Qualification	Doctor of Philosophy
Awarding Institution	The University of Western Australia
Supervisors/Advisors	Zheng, Minghao, Supervisor Pavlos, Nathan, Supervisor Cheng, Tak Sum, Supervisor
Award date	25 Sep 2017
DOIs	https://doi.org/10.4225/23/59d33d161fd5b
Publication status	Unpublished - 2017

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THESIS - DOCTOR OF PHILOSOPHY - GAO Junjie - 2017
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title = "Mechanisms underlying glucocorticoid-induced osteocyte dysfunction",

abstract = "The therapeutic functions of Glucocorticoids (GCs) are unfortunately accompanied by severe bone loss. Being the most abundant cell type in bone, osteocytes are highly susceptible to the adverse effects of GC treatment. In this thesis, the deleterious effects of GC on osteocytes and the underlying mechanisms governing these effects were explored and addressed: (1) GC regulates osteocyte-mediated bone modification and exosomal secretion; (2) GC impairs osteocyte communication by inducing autophagy-mediated degradation of Cx43; (3) GC inhibits ER-mediated mitochondrial transfer within the osteocyte processes; and (4) GC induces REDD1 to regulate autophagy via interaction with Akt-mTORC1 signalling.",

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N2 - The therapeutic functions of Glucocorticoids (GCs) are unfortunately accompanied by severe bone loss. Being the most abundant cell type in bone, osteocytes are highly susceptible to the adverse effects of GC treatment. In this thesis, the deleterious effects of GC on osteocytes and the underlying mechanisms governing these effects were explored and addressed: (1) GC regulates osteocyte-mediated bone modification and exosomal secretion; (2) GC impairs osteocyte communication by inducing autophagy-mediated degradation of Cx43; (3) GC inhibits ER-mediated mitochondrial transfer within the osteocyte processes; and (4) GC induces REDD1 to regulate autophagy via interaction with Akt-mTORC1 signalling.

AB - The therapeutic functions of Glucocorticoids (GCs) are unfortunately accompanied by severe bone loss. Being the most abundant cell type in bone, osteocytes are highly susceptible to the adverse effects of GC treatment. In this thesis, the deleterious effects of GC on osteocytes and the underlying mechanisms governing these effects were explored and addressed: (1) GC regulates osteocyte-mediated bone modification and exosomal secretion; (2) GC impairs osteocyte communication by inducing autophagy-mediated degradation of Cx43; (3) GC inhibits ER-mediated mitochondrial transfer within the osteocyte processes; and (4) GC induces REDD1 to regulate autophagy via interaction with Akt-mTORC1 signalling.

KW - Primary osteocyte

KW - Glucocorticoids

KW - Osteocyte communication

KW - Autophagy

KW - Exosomal secretion

KW - Mitochondrial transfer

KW - Akt-mTORC1 signalling

U2 - 10.4225/23/59d33d161fd5b

DO - 10.4225/23/59d33d161fd5b

M3 - Doctoral Thesis

ER -

Mechanisms underlying glucocorticoid-induced osteocyte dysfunction

Abstract

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