Neuropeptide calcitonin gene-related peptide (CGRP) is a neurotransmitter related to vasculogenesis during organ development. The vascular endothelial growth factor A (VEGF-A) is also required for vascular patterning during lung morphogenesis. CGRP is primarily found in organs and initially appears in pulmonary neuroendocrine cells during the early embryonic stage of lung development. However, the relationship between CGRP and VEGF-A during lung formation remains unclear. This study investigates CGRP and VEGF-A mRNA expressions in the embryonic, pseudoglandular, canalicular, saccular, and alveolar stages of lung development from embryonic day 12.5 (E12.5) to postnatal day 5 (P5) through quantitative real-time polymerase chain reaction (qRT-PCR) and in situ hybridization. Further, we analyzed the expression of CGRP via immunohistochemistry. The VEGF-A mRNA was mainly scattered across the whole lung body from E12.5. CGRP was found to be expressed in a few epithelial cells of the canalicular and the respiratory bronchiole of the lung from E12.5 to P5. An antisense probe for CGRP mRNA was strongly detected in the lung from E14.5 to E17.5. Endogenous CGRP may regulate the development of the embryonic alveoli from E14.5 to E17.5 in a temporal manner.

Background Learning and memory deficits and pathologic changes in the hippocampus caused by toothlessness and soft diet feeding are related to reduced masseter muscle (MM) function. Objective Myosin heavy chain (MyHC) isoform expression in the MM also changes under different chewing conditions. The neurotransmitter calcitonin gene‐related peptide (CGRP) and vascular endothelial growth factor A (VEGF‐A) are involved in MM formation. However, the relationship between CGRP, VEGF‐A and MyHC isoforms in the MM in the senescence‐accelerated mouse prone 8 (SAMP8) strain, a model of learning and memory deficits, remains unclear. Methods Changes in CGRP, VEGF‐A, vasculogenesis marker and MyHC isoform mRNA expression in the MMs of ageing SAMP8 and senescence‐accelerated mouse resistant 1 (SAMR1) mice was investigated through quantitative real‐time polymerase chain reaction (qRT–PCR) and in situ hybridization. Results qRT–PCR revealed obviously high CGRP levels in the SAMP8 mouse MM (p < .001). MyHC‐IId/x mRNA expression in the MM was higher in 24‐week‐old SAMP8 mice than 24‐week‐old SAMR1 mice (p < .001) but lower in slow‐MyHC SAMP8 mice than SAMR1 mice (p < .001). CGRP mRNA was observed on the muscle fibres of the SAMP8 mouse MM but not the SAMR1 mouse MM through in situ hybridization. Principal component analysis (PCA) revealed strong positive contributions of SAMP8‐MyHC‐IId/x, SAMP8‐CGRP, SAMR1‐MyHC‐emb, SAMR1‐CGRP, SAMR1‐VEGF‐A, SAMR1‐CD31, SAMP8‐VEGF‐A, and SAMP8‐CD31 in the MM at 12 and 24 weeks. Conclusion Calcitonin gene‐related peptide is also key for the MyHC‐IId/x and slow‐MyHC patterns in the MMs of SAMP8 mice.