CBP/p300-Interacting Protein CITED1 Modulates Parathyroid Hormone Regulation of Osteoblastic Differentiation

Yang, Dehong; Guo, Jun; Divieti, P.; Shioda, Toshi; Bringhurst, F. Richard

doi:10.1210/en.2007-0826

Cited by 31 publications

(27 citation statements)

References 21 publications

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“…Cell Culture-G s ␣(fl/fl) calvarial osteoblasts were harvested by serial collagenase digestion as described previously (47) and subjected to adenoviral infection with adeno-Cre or adeno-␤-galactosidase (35). Cells were plated at 5 ϫ 10 3 cells/cm 2 and induced to undergo osteogenic differentiation with ascorbic acid (50 g/ml) and ␤-glycerophosphate (10 mM).…”

Section: Methodsmentioning

confidence: 99%

Loss of Gsα in the Postnatal Skeleton Leads to Low Bone Mass and a Blunted Response to Anabolic Parathyroid Hormone Therapy

Sinha

Aarnisalo

Chubb

et al. 2016

Journal of Biological Chemistry

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. Surprisingly, in both male and female mice, PTH administration significantly increased osteoblast numbers and bone formation rate in both control and P-G s ␣ OsxKO mice. In mice that express a mutated PTH1R that activates adenylyl cyclase and protein kinase A (PKA) via G s ␣ but not phospholipase C via G q/11 (D/D mice), PTH significantly enhanced bone formation, indicating that phospholipase C activation is not required for increased bone turnover in response to PTH. Therefore, although the anabolic effect of intermittent PTH treatment on trabecular bone volume is blunted by deletion of G s ␣ in osteoblasts, PTH can stimulate osteoblast differentiation and bone formation. Together these findings suggest that alternative signaling pathways beyond G s ␣ and G q/11 act downstream of PTH on osteoblast differentiation.

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Section: Methodsmentioning

confidence: 99%

Loss of Gsα in the Postnatal Skeleton Leads to Low Bone Mass and a Blunted Response to Anabolic Parathyroid Hormone Therapy

Sinha

Aarnisalo

Chubb

et al. 2016

Journal of Biological Chemistry

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“…Primary calvarial osteoblastic cells were isolated from wild-type mice at postnatal day 6 by serial collagenase digestion [41]. Adherent cells were plated at 12,500 cells/cm2 and osteogenic differentiation induced with 10 mM β-glycerol phosphate and 50 μg/ml ascorbic acid.…”

Section: Methodsmentioning

confidence: 99%

Potent constitutive cyclic AMP-generating activity of XLαs implicates this imprinted GNAS product in the pathogenesis of McCune–Albright Syndrome and fibrous dysplasia of bone

Mariot¹,

Wu²,

Aydın³

et al. 2011

Bone

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Patients with McCune-Albright syndrome (MAS), characterized primarily by hyperpigmented skin lesions, precocious puberty, and fibrous dyslasia of bone, carry postzygotic heterozygous mutations of GNAS causing constitutive cAMP signaling. GNAS encodes the α-subunit of the stimulatory G protein (Gsα), as well as a large variant (XLαs) derived from the paternal allele. The mutations causing MAS affect both GNAS products, but whether XLαs, like Gsα, can be involved in the pathogenesis remains unknown. Here, we investigated biopsy samples from four previously reported and eight new patients with MAS. Activating mutations of GNAS (Arg201 with respect to the amino acid sequence of Gsα) were present in all the previously reported and five of the new cases. The mutation was detected within the paternally expressed XLαs transcript in five and the maternally expressed NESP55 transcript in four cases. Tissues carrying paternal mutations appeared to have higher XLαs mRNA levels than maternal mutations. The human XLαs mutant analogous to Gsα-R201H (XLαs-R543H) showed markedly higher basal cAMP accumulation than wild-type XLαs in transfected cells. Wild-type XLαs demonstrated higher basal and isoproterenol-induced cAMP signaling than Gsα and co-purified with Gβ1γ2 in transduced cells. XLαs mRNA was measurable in mouse calvarial cells, with its level being significantly higher in undifferentiated cells than those expressing preosteoblastic markers osterix and alkaline phosphatase. XLαs mRNA was also expressed in murine bone marrow stromal cells and preosteoblastic MC3T3-E1 cells. Our findings are consistent with the possibility that constitutive XLαs activity adds to the molecular pathogenesis of MAS and fibrous dysplasia of bone.

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“…OsxKO and control (Osx1-GFP::Cre ϩ ; Gs␣ ϩ/ϩ ) mice by serial collagenase digestion (37). Fractions 3-6 were pooled and resuspended in phosphate-buffered saline (PBS) with 2% fetal bovine serum.…”

Section: Isolation Of Osteoblastic Cells By Facs Osteoblastic Cells mentioning

confidence: 99%

Osteoblastic regulation of B lymphopoiesis is mediated by G _s α-dependent signaling pathways

Purton

Rodda

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

233

202

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CBP/p300-Interacting Protein CITED1 Modulates Parathyroid Hormone Regulation of Osteoblastic Differentiation

Cited by 31 publications

References 21 publications

Loss of Gsα in the Postnatal Skeleton Leads to Low Bone Mass and a Blunted Response to Anabolic Parathyroid Hormone Therapy

Loss of Gsα in the Postnatal Skeleton Leads to Low Bone Mass and a Blunted Response to Anabolic Parathyroid Hormone Therapy

Potent constitutive cyclic AMP-generating activity of XLαs implicates this imprinted GNAS product in the pathogenesis of McCune–Albright Syndrome and fibrous dysplasia of bone

Osteoblastic regulation of B lymphopoiesis is mediated by G _s α-dependent signaling pathways

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CBP/p300-Interacting Protein CITED1 Modulates Parathyroid Hormone Regulation of Osteoblastic Differentiation

Cited by 31 publications

References 21 publications

Loss of Gsα in the Postnatal Skeleton Leads to Low Bone Mass and a Blunted Response to Anabolic Parathyroid Hormone Therapy

Loss of Gsα in the Postnatal Skeleton Leads to Low Bone Mass and a Blunted Response to Anabolic Parathyroid Hormone Therapy

Potent constitutive cyclic AMP-generating activity of XLαs implicates this imprinted GNAS product in the pathogenesis of McCune–Albright Syndrome and fibrous dysplasia of bone

Osteoblastic regulation of B lymphopoiesis is mediated by G s α-dependent signaling pathways

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Osteoblastic regulation of B lymphopoiesis is mediated by G _s α-dependent signaling pathways