Prostaglandin F2 receptor (FP) signaling regulates Bmp signaling and promotes chondrocyte differentiation

Kim, Joohwee; Shim, Minsub

doi:10.1016/j.bbamcr.2014.12.003

Cited by 11 publications

(9 citation statements)

References 46 publications

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“…Previous studies showed that PGF2α stimulated the expression of cartilage marker genes in a rat cell line and human articular chondrocytes [29,30]. Studies also revealed that PTGFR participates in chondrocyte hypertrophy differentiation by regulating Bmp signaling [27]. Therefore, PTGFR may affect hip joint development as a receptor of PGF2α, which promotes cartilage formation.…”

Section: Discussionmentioning

confidence: 96%

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Replicative Verification of Susceptibility Genes Previously Identified from Families with Segregating Developmental Dysplasia of the Hip

Wang²,

Chen

et al. 2020

Preprint

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Background: Developmental dysplasia of the hip (DDH) is a complex hip joint deformity with effects ranging from acetabulum malformation to irreversible hip dislocation. Previous studies suggest a significant association of four variations, Teneurin transmembrane protein 3 (TENM3) (chr4:183721398), Heparan sulfate proteoglycan 2 (HSPG2) (chr1:22201470), ATPase plasma membrane Ca2+ transporting 4 (ATP2B4) (chr1:203682345), and Prostaglandin F receptor (PTGFR) (chr1:79002214), with DDH susceptibility in families with segregating DDH. However, the association was not validated in sporadic cases and remains controversial. To confirm the association of the reported variations in these four genes with DDH, we conducted replicative verification in 250 sporadic samples with DDH from a Chinese Han population. Methods: We conducted Sanger sequencing after amplifying the variation sites. The results were compared with the reference sequence from the GRCh37 assembly in UCSC (http://genome.ucsc.edu). Results: Replication analysis of 250 sporadic samples by Sanger sequencing indicated that the four variations, TENM3 (chr4:183721398), HSPG2 (chr1:22201470), ATP2B4 (chr1:203682345), and PTGFR (chr1:79002214), were not associated with the susceptibility to DDH in the Chinese Han population.Conclusions: Further studies should be performed to identify other variations of these four genes that are potentially associated with DDH by whole-exome sequencing and the results should be verified in different populations.

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Section: Discussionmentioning

confidence: 96%

“…PTGFR, also known as FP, belongs to the G protein-coupled receptor family of seven transmembranespanning receptors. PTGFR plays an important role in chondrocyte differentiation and cartilage development [26][27][28]. PGF2α exerts its biological activities by binding to its receptor, PTGFR [29].…”

Section: Discussionmentioning

confidence: 99%

Replicative Verification of Susceptibility Genes Previously Identified from Families with Segregating Developmental Dysplasia of the Hip

Wang²,

Chen

et al. 2020

Preprint

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“…PTGFR (OMIM * 600563) , also known as FP, belongs to the G protein-coupled receptor family of seven transmembrane-spanning receptors. PTGFR plays an important role in chondrocyte differentiation and cartilage development [27][28][29]. PGF2α exerts its biological activities by binding to its receptor, PTGFR [30].…”

Section: Discussionmentioning

confidence: 99%

Replicative Verification of Susceptibility Genes Previously Identified from Families with Segregating Developmental Dysplasia of the Hip

Wang²,

Chen

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Developmental dysplasia of the hip (DDH) is a complex hip joint deformity with effects ranging from acetabulum malformation to irreversible hip dislocation. Previous studies suggest a significant association of four variations, teneurin transmembrane protein 3 (TENM3, OMIM * 610083) (chr4:183721398), heparan sulfate proteoglycan 2 (HSPG2, OMIM * 142461 ) (chr1:22201470), ATPase plasma membrane Ca2+ transporting 4 (ATP2B4, OMIM * 108732) (chr1:203682345), and prostaglandin F receptor (PTGFR, OMIM * 600563) (chr1:79002214), with DDH susceptibility in families with segregating DDH. However, the association was not validated in sporadic cases and remains controversial. To confirm the association of the reported variations in these four genes with DDH, we conducted replicative verification in 250 sporadic samples with DDH from a Chinese Han population. Methods: We conducted Sanger sequencing after amplifying the variation sites. The results were compared with the reference sequence from the GRCh37 assembly in UCSC (http://genome.ucsc.edu). Results: Replication analysis of 250 sporadic samples by Sanger sequencing indicated that the four variations, TENM3 (OMIM * 610083, chr4:183721398), HSPG2 (OMIM * 142461, chr1:22201470), ATP2B4 (OMIM * 108732, chr1:203682345), and PTGFR (OMIM * 600563, chr1:79002214), were not associated with the susceptibility to DDH in the Chinese Han population.Conclusions: Further studies should be performed to identify other variations of these four genes that are potentially associated with DDH by whole-exome sequencing and the results should be verified in different populations.

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“…In addition, COX2 has been shown to regulate mesenchymal cell differentiation into osteoblast lineage [50]. We have also recently shown that prostaglandin F 2ɑ (PGF 2ɑ ) stimulates chondrocyte differentiation and promotes bone morphogenetic protein (BMP) signaling [51]. Thus, increased expression of COX2 may protect the skeleton from age-associated damage such as osteo-porosis, which is frequently observed in other mouse models of aging.…”

Section: Discussionmentioning

confidence: 99%

Transgenic expression of cyclooxygenase-2 (COX2) causes premature aging phenotypes in mice

Kim

Vaish

Feng

et al. 2016

Aging

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Cyclooxygenase (COX) is a key enzyme in the biosynthesis of prostanoids, lipid signaling molecules that regulate various physiological processes. COX2, one of the isoforms of COX, is highly inducible in response to a wide variety of cellular and environmental stresses. Increased COX2 expression is thought to play a role in the pathogenesis of many age-related diseases. COX2 expression is also reported to be increased in the tissues of aged humans and mice, which suggests the involvement of COX2 in the aging process. However, it is not clear whether the increased COX2 expression is causal to or a result of aging. We have now addressed this question by creating an inducible COX2 transgenic mouse model. Here we show that post-natal expression of COX2 led to a panel of aging-related phenotypes. The expression of p16, p53, and phospho-H2AX was increased in the tissues of COX2 transgenic mice. Additionally, adult mouse lung fibroblasts from COX2 transgenic mice exhibited increased expression of the senescence-associated β-galactosidase. Our study reveals that the increased COX2 expression has an impact on the aging process and suggests that modulation of COX2 and its downstream signaling may be an approach for intervention of age-related disorders.

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Prostaglandin F2 receptor (FP) signaling regulates Bmp signaling and promotes chondrocyte differentiation

Cited by 11 publications

References 46 publications

Replicative Verification of Susceptibility Genes Previously Identified from Families with Segregating Developmental Dysplasia of the Hip

Replicative Verification of Susceptibility Genes Previously Identified from Families with Segregating Developmental Dysplasia of the Hip

Replicative Verification of Susceptibility Genes Previously Identified from Families with Segregating Developmental Dysplasia of the Hip

Transgenic expression of cyclooxygenase-2 (COX2) causes premature aging phenotypes in mice

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