Spexin Enhances Bowel Movement through Activating L-type Voltage-dependent Calcium Channel via Galanin Receptor 2 in Mice

Cheng Yuan Lin; Man Zhang; Tao Huang; Li Ling Yang; Hai Bo Fu; Ling Zhao; Lidan ZHONG; Huai Xue Mu; Xiao Ke Shi; Christina Fp Leung; Bao Min Fan; Miao Jiang; Aiping Lu; Li Xin Zhu; Zhaoxiang BIAN

doi:10.1038/srep12095

Spexin Enhances Bowel Movement through Activating L-type Voltage-dependent Calcium Channel via Galanin Receptor 2 in Mice

Cheng Yuan Lin, Man Zhang, Tao Huang, Li Ling Yang, Hai Bo Fu, Ling Zhao, Lidan ZHONG, Huai Xue Mu, Xiao Ke Shi, Christina Fp Leung, Bao Min Fan, Miao Jiang, Aiping Lu, Li Xin Zhu, Zhaoxiang BIAN^*

^*Corresponding author for this work

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Abstract

A novel neuropeptide spexin was found to be broadly expressed in various endocrine and nervous tissues while little is known about its functions. This study investigated the role of spexin in bowel movement and the underlying mechanisms. In functional constipation (FC) patients, serum spexin levels were significantly decreased. Consistently, in starved mice, the mRNA of spexin was significantly decreased in intestine and colon. Spexin injection increased the velocity of carbon powder propulsion in small intestine and decreased the glass beads expulsion time in distal colon in mice. Further, spexin dose-dependently stimulated the intestinal/colonic smooth muscle contraction. Galanin receptor 2 (GALR2) antagonist M871, but not Galanin receptor 3 (GALR3) antagonist SNAP37899, effectively suppressed the stimulatory effects of spexin on intestinal/colonic smooth muscle contraction, which could be eliminated by extracellular [Ca²⁺] removal and L-type voltage-dependentCa²⁺ channel (VDCC) inhibitor nifedipine. Besides, spexin dramatically increased the [Ca²⁺]i in isolated colonic smooth muscle cells. These data indicate that spexin can act on GALR2 receptor to regulate bowel motility by activating L-type VDCC. Our findings provide evidence for important physiological roles of spexin in GI functions. Selective action on spexin pathway might have therapeutic effects on GI diseases with motility disorders.

Original language	English
Article number	12095
Journal	Scientific Reports
Volume	5
DOIs	https://doi.org/10.1038/srep12095
Publication status	Published - 10 Jul 2015

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Lin, C. Y., Zhang, M., Huang, T., Yang, L. L., Fu, H. B., Zhao, L., ZHONG, L., Mu, H. X., Shi, X. K., Leung, C. F., Fan, B. M., Jiang, M., Lu, A., Zhu, L. X., & BIAN, Z. (2015). Spexin Enhances Bowel Movement through Activating L-type Voltage-dependent Calcium Channel via Galanin Receptor 2 in Mice. Scientific Reports, 5, Article 12095. https://doi.org/10.1038/srep12095

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title = "Spexin Enhances Bowel Movement through Activating L-type Voltage-dependent Calcium Channel via Galanin Receptor 2 in Mice",

abstract = "A novel neuropeptide spexin was found to be broadly expressed in various endocrine and nervous tissues while little is known about its functions. This study investigated the role of spexin in bowel movement and the underlying mechanisms. In functional constipation (FC) patients, serum spexin levels were significantly decreased. Consistently, in starved mice, the mRNA of spexin was significantly decreased in intestine and colon. Spexin injection increased the velocity of carbon powder propulsion in small intestine and decreased the glass beads expulsion time in distal colon in mice. Further, spexin dose-dependently stimulated the intestinal/colonic smooth muscle contraction. Galanin receptor 2 (GALR2) antagonist M871, but not Galanin receptor 3 (GALR3) antagonist SNAP37899, effectively suppressed the stimulatory effects of spexin on intestinal/colonic smooth muscle contraction, which could be eliminated by extracellular [Ca2+] removal and L-type voltage-dependentCa2+ channel (VDCC) inhibitor nifedipine. Besides, spexin dramatically increased the [Ca2+]i in isolated colonic smooth muscle cells. These data indicate that spexin can act on GALR2 receptor to regulate bowel motility by activating L-type VDCC. Our findings provide evidence for important physiological roles of spexin in GI functions. Selective action on spexin pathway might have therapeutic effects on GI diseases with motility disorders.",

author = "Lin, {Cheng Yuan} and Man Zhang and Tao Huang and Yang, {Li Ling} and Fu, {Hai Bo} and Ling Zhao and Lidan ZHONG and Mu, {Huai Xue} and Shi, {Xiao Ke} and Leung, {Christina Fp} and Fan, {Bao Min} and Miao Jiang and Aiping Lu and Zhu, {Li Xin} and Zhaoxiang BIAN",

note = "Funding Information: This study was supported by Food and Health Bureau, Hong Kong, China, through its Health and Health Services Research Fund (project no. 09101501) and Hong Kong Baptist University, Hong Kong, China, through its Faculty Research Grant (project no. FRG2/14-15/001).",

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AU - Zhang, Man

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AU - Fu, Hai Bo

AU - Zhao, Ling

AU - ZHONG, Lidan

AU - Mu, Huai Xue

AU - Shi, Xiao Ke

AU - Leung, Christina Fp

AU - Fan, Bao Min

AU - Jiang, Miao

AU - Lu, Aiping

AU - Zhu, Li Xin

AU - BIAN, Zhaoxiang

N1 - Funding Information: This study was supported by Food and Health Bureau, Hong Kong, China, through its Health and Health Services Research Fund (project no. 09101501) and Hong Kong Baptist University, Hong Kong, China, through its Faculty Research Grant (project no. FRG2/14-15/001).

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N2 - A novel neuropeptide spexin was found to be broadly expressed in various endocrine and nervous tissues while little is known about its functions. This study investigated the role of spexin in bowel movement and the underlying mechanisms. In functional constipation (FC) patients, serum spexin levels were significantly decreased. Consistently, in starved mice, the mRNA of spexin was significantly decreased in intestine and colon. Spexin injection increased the velocity of carbon powder propulsion in small intestine and decreased the glass beads expulsion time in distal colon in mice. Further, spexin dose-dependently stimulated the intestinal/colonic smooth muscle contraction. Galanin receptor 2 (GALR2) antagonist M871, but not Galanin receptor 3 (GALR3) antagonist SNAP37899, effectively suppressed the stimulatory effects of spexin on intestinal/colonic smooth muscle contraction, which could be eliminated by extracellular [Ca2+] removal and L-type voltage-dependentCa2+ channel (VDCC) inhibitor nifedipine. Besides, spexin dramatically increased the [Ca2+]i in isolated colonic smooth muscle cells. These data indicate that spexin can act on GALR2 receptor to regulate bowel motility by activating L-type VDCC. Our findings provide evidence for important physiological roles of spexin in GI functions. Selective action on spexin pathway might have therapeutic effects on GI diseases with motility disorders.

AB - A novel neuropeptide spexin was found to be broadly expressed in various endocrine and nervous tissues while little is known about its functions. This study investigated the role of spexin in bowel movement and the underlying mechanisms. In functional constipation (FC) patients, serum spexin levels were significantly decreased. Consistently, in starved mice, the mRNA of spexin was significantly decreased in intestine and colon. Spexin injection increased the velocity of carbon powder propulsion in small intestine and decreased the glass beads expulsion time in distal colon in mice. Further, spexin dose-dependently stimulated the intestinal/colonic smooth muscle contraction. Galanin receptor 2 (GALR2) antagonist M871, but not Galanin receptor 3 (GALR3) antagonist SNAP37899, effectively suppressed the stimulatory effects of spexin on intestinal/colonic smooth muscle contraction, which could be eliminated by extracellular [Ca2+] removal and L-type voltage-dependentCa2+ channel (VDCC) inhibitor nifedipine. Besides, spexin dramatically increased the [Ca2+]i in isolated colonic smooth muscle cells. These data indicate that spexin can act on GALR2 receptor to regulate bowel motility by activating L-type VDCC. Our findings provide evidence for important physiological roles of spexin in GI functions. Selective action on spexin pathway might have therapeutic effects on GI diseases with motility disorders.

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Spexin Enhances Bowel Movement through Activating L-type Voltage-dependent Calcium Channel via Galanin Receptor 2 in Mice

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