Cloning, sequencing and tissue distribution of two related G protein‐coupled receptor candidates expressed prominently in human lung tissue

An, Songzhu; Tsai, Cannit; Goetzl, Edward J.

doi:10.1016/0014-5793(95)01196-l

Cited by 29 publications

(16 citation statements)

References 20 publications

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“…Human RNA Master Blot Probed with GPR4 -GPR4 has been shown to be expressed in many human tissues (18). For a wider analysis of GPR4 expression in human tissues, we probed the Human RNA Master Blot (CLONTECH) containing RNAs from 50 different human tissues with the full-length human GPR4 clone labeled with [ 32 P]dCTP ("Experimental Procedures").…”

Section: Resultsmentioning

confidence: 99%

“…Whereas GPR4 is expressed at high levels, in the liver, kidney, and ovary ( Fig. 1), OGR1 is not expressed in these tissues (8,18). The physiological and pathological roles of these receptors remain to be further investigated.…”

Section: Discussionmentioning

confidence: 98%

“…Both OGR1 and GPR4 are highly expressed in the lung. However, OGR1 is expressed at high levels in the placenta, spleen, testis, small intestine, and peripheral leukocytes (8,18), whereas GPR4 is not expressed, or is expressed at relatively low levels, in these tissues. Whereas GPR4 is expressed at high levels, in the liver, kidney, and ovary ( Fig.…”

Section: Discussionmentioning

confidence: 99%

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Sphingosylphosphorylcholine and Lysophosphatidylcholine Are Ligands for the G Protein-coupled Receptor GPR4

Zhu¹,

Baudhuin²,

Hong³

et al. 2001

Journal of Biological Chemistry

223

166

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Sphingosylphosphorylcholine (SPC) and lysophosphatidylcholine (LPC) are bioactive lipid molecules involved in numerous biological processes. We have recently identified ovarian cancer G protein-coupled receptor 1 (OGR1) as a specific and high affinity receptor for SPC, and G2A as a receptor with high affinity for LPC, but low affinity for SPC. Among G protein-coupled receptors, GPR4 shares highest sequence homology with OGR1 (51%). In this work, we have identified GPR4 as not only another high affinity receptor for SPC, but also a receptor for LPC, albeit of lower affinity. Both Taken together, our data indicate that GPR4 is a receptor with high affinity to SPC and low affinity to LPC, and that multiple cellular functions can be transduced via this receptor.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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Sphingosylphosphorylcholine and Lysophosphatidylcholine Are Ligands for the G Protein-coupled Receptor GPR4

Zhu¹,

Baudhuin²,

Hong³

et al. 2001

Journal of Biological Chemistry

223

166

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“…GPR65 and GPR68 are predominately, though not exclusively, expressed on leukocytes and provide various roles in the exacerbation or amelioration of a diverse set of diseases associated with inflammation and acidosis [1, 11]. GPR4, reciprocally, is highly expressed in vascular endothelial cells (ECs) and blood vessel rich tissues such as the lung, kidney, heart, and liver [9, 12–14]. Recently, GPR4 has been shown to mediate EC inflammatory responses to acidosis and is central for leukocyte-endothelium interaction [15, 16].…”

Section: Introductionmentioning

confidence: 99%

GPR4 deficiency alleviates intestinal inflammation in a mouse model of acute experimental colitis

Sanderlin

Leffler

Lertpiriyapong

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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GPR4 is a proton-sensing G protein-coupled receptor that can be activated by extracellular acidosis. It has recently been demonstrated that activation of GPR4 by acidosis increases the expression of numerous inflammatory and stress response genes in vascular endothelial cells (ECs) and also augments EC-leukocyte adhesion. Inhibition of GPR4 by siRNA or small molecule inhibitors reduces endothelial cell inflammation. As acidotic tissue microenvironments exist in many types of inflammatory disorders, including inflammatory bowel disease (IBD), we examined the role of GPR4 in intestinal inflammation using a dextran sulfate sodium (DSS)-induced acute colitis mouse model. We observed that GPR4 mRNA expression was increased in mouse and human IBD tissues when compared to control intestinal tissues. To determine the function of GPR4 in intestinal inflammation, wild-type and GPR4-deficient mice were treated with 3% DSS for 7 days to induce acute colitis. Our results showed that the severity of colitis was decreased in GPR4-deficient DSS-treated mice in comparison to wild-type DSS-treated mice. Clinical parameters, macroscopic disease indicators, and histopathological features were less severe in the DSS-treated GPR4-deficient mice than the DSS-treated wild-type mice. Endothelial adhesion molecule expression, leukocyte infiltration, and isolated lymphoid follicle (ILF) formation were reduced in intestinal tissues of DSS-treated GPR4-null mice. Collectively, our results suggest GPR4 provides a pro-inflammatory role in the inflamed gut as the absence of GPR4 ameliorates intestinal inflammation in the acute experimental colitis mouse model.

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“…Studies have shown that GPR4 is expressed in vascular endothelial and smooth muscle cells, lung, kidney, heart, liver, and other tissues (1,23,35,36,51). The in vivo function of GPR4 is not well understood, although recent studies indicate that GPR4-related genes in Xenopus laevis are involved in the regulation of embryonic gastrulation (8,49).…”

mentioning

confidence: 99%

Vascular Abnormalities in Mice Deficient for the G Protein-Coupled Receptor GPR4 That Functions as a pH Sensor

Yang

Radu²,

Roy³

et al. 2007

Molecular and Cellular Biology

113

141

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GPR4 is a G protein-coupled receptor expressed in the vasculature, lung, kidney, and other tissues. In vitro ectopic overexpression studies implicated GPR4 in sensing extracellular pH changes leading to cyclic AMP (cAMP) production. To investigate its biological roles in vivo, we generated GPR4-deficient mice by homologous recombination. Whereas GPR4-null adult mice appeared phenotypically normal, neonates showed a higher frequency of perinatal mortality. The average litter size from GPR4 ؊/؊ intercrosses was ϳ30% smaller than that from GPR4 ؉/؉ intercrosses on N3 and N5 C57BL/6 genetic backgrounds. A fraction of knockout embryos and neonates had spontaneous hemorrhages, dilated and tortuous subcutaneous blood vessels, and defective vascular smooth muscle cell coverage. Mesangial cells in kidney glomeruli were also significantly reduced in GPR4-null neonates. Some neonates exhibited respiratory distress with airway lining cell metaplasia. To examine whether GPR4 is functionally involved in vascular pH sensing, an ex vivo aortic ring assay was used under defined pH conditions. Compared to wild-type aortas, microvessel outgrowth from GPR4-null aortas was less inhibited by acidic extracellular pH. Treatment with an analog of cAMP, a downstream effector of GPR4, abolished microvessel outgrowth bypassing the GPR4-knockout phenotype. These results suggest that GPR4 deficiency leads to partially penetrant vascular abnormalities during development and that this receptor functions in blood vessel pH sensing.

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Cloning, sequencing and tissue distribution of two related G protein‐coupled receptor candidates expressed prominently in human lung tissue

Cited by 29 publications

References 20 publications

Sphingosylphosphorylcholine and Lysophosphatidylcholine Are Ligands for the G Protein-coupled Receptor GPR4

Sphingosylphosphorylcholine and Lysophosphatidylcholine Are Ligands for the G Protein-coupled Receptor GPR4

GPR4 deficiency alleviates intestinal inflammation in a mouse model of acute experimental colitis

Vascular Abnormalities in Mice Deficient for the G Protein-Coupled Receptor GPR4 That Functions as a pH Sensor

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