Expression of CGRP in embryonic mouse masseter muscle

Azuma, Yuri; Miwa, Yoko; Sato, Iwao

doi:10.1016/j.aanat.2016.04.031

Cited by 8 publications

(14 citation statements)

References 29 publications

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“…These results are consistent with those of a previous study showing that CGRP expression is associated with blood vessels during the formation of the mouse masseter muscle. 37 In the present study, during bone matrix formation, CGRP expression around the blood vessels started at E14.5 in the mandible and E17.5 in the tibia. In general, CGRP is widely distributed in the bone tissue and regulates bone remodelling through blood vessels around bone cells during growth and repair.…”

Section: Discussionsupporting

confidence: 51%

“…CGRP may regulate VEGF-A expression, and subsequently VEGF-A may be upregulated as an intermediate pathway for vascular endothelial cells and induced CD31. 37 Therefore, a time lag of expression was observed between the mandible and tibia during foetal development. These results also showed that the pattern of OPN hybridization with the anti-sense probe was similar to that of CGRP in the tibia and mandible.…”

Section: Discussionmentioning

confidence: 99%

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Expression of CGRP, vasculogenesis and osteogenesis associated mRNAs in the developing mouse mandible and tibia

2017

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The neuropeptide Calcitonin Gene-Related Peptide (CGRP) is a well-characterized neurotransmitter. However, little is known about the role of CGRP in osteogenesis and vascular genesis during the developmental formation of bone. In the present study, we assessed the abundance of CGRP mRNA and the mRNA of osteogenesis and vascular genesis markers in the foetal mouse mandible and leg bone (tibia). We also analysed the expression and localization of CGRP, osteopontin (OPN) and vascular endothelial growth factor (VEGF-A) using in situ hybridization and immunohistochemical localization in the mouse mandible and tibia at embryonic days 12.5 (E12.5), E14.5, E17.5, and postnatal day 1 (P1). CGRP was clearly detected in the mandible relative to the tibia at E14.5. Hybridization using an anti-sense probe for CGRP was not detected in the mandible at P1. Hybridization with an anti-sense probe for OPN was detected at E14.5, later in the mandible and at P1 in Meckel’s cartilage. However, OPN was only detected in the tibia at E17.5 and later. The abundance of CGRP mRNA differed between the mandible and tibia. The level of vasculogenesis markers, such as VEGF-A, was similar to that of CGRP in the mandible. The levels of VEGF-A, cluster of differentiation 31 (CD31) and lymphatic vessel endothelial hyaluronan receptor 1 (LIVE-1) differed from that of OPN in the mandible. In contrast, the levels of VEGF-A, CD31, matrix metalloproteinase-2 (MMP-2), collagen I (Col I), collagen II (Col II) and OPN mRNA differed from E12.5 to P1 (P<0.001) in the tibia. The abundance of mRNA of CGRP and bone matrix markers (Col I, Col II, and OPN) was low at P5 in the tibia. These differences in CGRP and other mRNAs may induce a different manner of ossification between the mandible and tibia. Therefore, a time lag of ossification occurs between the mandible and tibia during foetal development.

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Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Expression of CGRP, vasculogenesis and osteogenesis associated mRNAs in the developing mouse mandible and tibia

2017

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“…Neurons in the SCG undergo maturation and differentiation from E14.5 to P1 during development. According to Azuma reports, 22 the expression of CGRP mRNA peaks at E17.5 in the mouse masseter muscle in response to the shift from embryonic MyHCs to adult MyHCs at E17.5. Moreover, the peak expression of CGRP mRNA was detected at E17.5 in the mouse tibia and at P0 in the mouse mandible.…”

Section: Discussionmentioning

confidence: 98%

Localization of CGRP and VEGF mRNAs in the mouse superior cervical ganglion during pre- and postnatal development

Mitsuoka¹,

Miwa²,

Kikutani³

et al. 2018

Eur J Histochem

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The neuropeptide calcitonin gene-related peptide (CGRP) mediates inflammation and head pain by influencing the functional vascular blood supply. CGRP is a well-characterized mediator of receptor-regulated neurotransmitter release. However, knowledge regarding the role of CGRP during the development of the superior cervical ganglion (SCG) is limited. In the present study, we observed the localization of CGRP and vascular endothelial growth factor (VEGFA) mRNAs during prenatal development at embryonic day 14.5 (E14.5), E17.5 and postnatal day 1 (P1) using in situ hybridization. The antisense probe for CGRP was detected by in situ hybridization at E14.5, E17.5, and P1, and the highest levels were detected at E17.5. In contrast, the antisense probe for VEGF-A was detected by in situ hybridization in gradually increasing intensity from E14.5 to P1. The differences in the expression of these two markers revealed specific characteristics related to CGRP concentration and release compared to those of VEGF-A during development. The correlation between CGRP and VEGF-A may influence functional stress and the vascular blood supply during prenatal and postnatal development.

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“…The previous clinical study proved that hyperoxia inhalation causes BPD [ 23 ], which mainly results from AEC II cell proliferation induced by hyperoxia [ 24 , 25 ]. CGRP is a cell regulatory factor and extra-cellular signal molecule, which is also closely associated with embryonic development and cell proliferation [ 26 ]. Therefore, in this study, we investigated the effects of heterologously expressed CGRP on AEC II cells apoptosis and anti-oxidative activity, as well as Notch 1 and HERP expression.…”

Section: Discussionmentioning

confidence: 99%

Extrinsic Calcitonin Gene-Related Peptide Inhibits Hyperoxia-Induced Alveolar Epithelial Type II Cells Apoptosis, Oxidative Stress, and Reactive Oxygen Species (ROS) Production by Enhancing Notch 1 and Homocysteine-Induced Endoplasmic Reticulum Protein (HERP) Expression

et al. 2017

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BackgroundLung alveolar epithelial type II cells (AEC II) are the most important stem cells in lung tissues, which are critical for wound repair of bronchopulmonary dysplasia (BPD). This study investigated the effects of calcitonin gene-related peptide (CGRP) on AEC II cells exposed to hyperoxia.Material/MethodsNeonatal rat AEC II cells were isolated and identified by detecting surfactant protein C (SP-C). Three small interfering RNAs targeting Notch 1 were synthesized and transfected into AEC II. A hyperoxia-exposed AEC II cell injury model was established and was divided into 8 groups. MDA levels and SOD activity were examined using lipid peroxidation assay kits. Apoptosis and reactive oxygen species (ROS) production were evaluated using flow cytometry. Notch 1 mRNA expression was examined using RT-PCR. Homocysteine-induced endoplasmic reticulum protein (HERP) was examined using Western blot analysis.ResultsCGRP treatment significantly enhanced MDA levels and decreased SOD activity compared to hyperoxia-treated AEC II cells (P<0.05). CGRP treatment significantly inhibited hyperoxia-induced AEC II cell apoptosis, and significantly suppressed hyperoxia-induced ROS production compared to hyperoxia-treated AEC II cells (P<0.05) either undergoing γ secretase inhibitor or Notch RNA interference. CGRP significantly triggered Notch 1 mRNA expression and significantly enhanced HERP expression compared to hyperoxia-treated AEC II cells (P<0.05) either undergoing γ secretase inhibitor or Notch RNA interference.ConclusionsIn AEC II cells, extrinsic peptide CGRP suppressed hyperoxia-induced apoptosis, oxidative stress, and ROS production, which may be triggered by Notch 1 and HERP signaling pathway.

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Expression of CGRP in embryonic mouse masseter muscle

Cited by 8 publications

References 29 publications

Expression of CGRP, vasculogenesis and osteogenesis associated mRNAs in the developing mouse mandible and tibia

Expression of CGRP, vasculogenesis and osteogenesis associated mRNAs in the developing mouse mandible and tibia

Localization of CGRP and VEGF mRNAs in the mouse superior cervical ganglion during pre- and postnatal development

Extrinsic Calcitonin Gene-Related Peptide Inhibits Hyperoxia-Induced Alveolar Epithelial Type II Cells Apoptosis, Oxidative Stress, and Reactive Oxygen Species (ROS) Production by Enhancing Notch 1 and Homocysteine-Induced Endoplasmic Reticulum Protein (HERP) Expression

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