Abstract

Hypertension is a systemic disorder that affects numerous physiological processes throughout the body. Improper sodium transport is a common comorbidity of hypertension, and sodium transport is also critical for maintaining the secretion of submandibular glands, whether the function of submandibular glands is affected by hypertension remains unclear. To determine whether hypertension induces changes in the protein expression of submandibular glands, we compared the proteome of submandibular glands from 14-week-old spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats using LC-MS/MS. The results revealed that 95 proteins displayed different levels of expression between the submandibular glands from the SHRs and WKYs. Among these, 35 proteins were more abundant, and 60 proteins were less abundant in the SHR compared with the WKY rats. Specifically, aquaporin 5 and parvalbumin, which are correlated with water transport and intracellular Ca2+ signal transduction, were verified to exhibit differences in protein abundance. Impaired Ca2+ response to carbachol was confirmed in the acinar cells from SHRs, and hyposecretion by the submandibular glands was further confirmed by in vivo saliva collection. In conclusion, the proteomic analysis of the submandibular glands of SHRs revealed novel changes in protein abundance that provides possible mechanisms connecting hypertension and hyposecretion in submandibular glands.

Highlights

  • Hypertension, known as high blood pressure, is a long-term systemic disorder that affects numerous physiological processes throughout the body

  • A profile plot of the differentially expressed proteins with categorical annotation (Fig. 1A) revealed that the up-regulated proteins in the spontaneously hypertensive rat (SHR) group were involved in the KEGG pathway of N-glycan biosynthesis, arginine and proline metabolism, a MAPK signaling pathway, cysteine and methionine metabolism, glycine, serine and threonine metabolism, and calcium signaling pathways, whereas the down-regulated proteins were involved in salivary secretion, amino sugar and nucleotide sugar metabolism, the adipocytokine signaling pathway, retinol metabolism, aldosterone-regulated sodium reabsorption, and glycine, serine and threonine metabolism

  • We investigated the extent to which hypertension affected submandibular glands (SMGs) protein expression and salivation

Read more

Summary

Introduction

Hypertension, known as high blood pressure, is a long-term systemic disorder that affects numerous physiological processes throughout the body. The infusion of angiotensin II into the parotid gland via the carotid artery causes a substantial reduction in the saliva secretion rate, which suggests a direct inhibitory effect of angiotensin II on the parotid that is possibly mediated by a constricting action on its vasculature or alters in water and electrolyte transport[11]. The spontaneously hypertensive rat (SHR) is the most widely used animal model of essential hypertension and its accompanying metabolic disturbances when under special environmental conditions (for example, when fed a high-fructose or folate-deficient diet)[14]. The aim of this study was to apply a proteomic approach to identify altered proteins and pathways involved in salivation in the submandibular glands (SMGs) of SHRs compared with those in WKY. We further confirmed an impaired Ca2+ signal, a reduced abundance of AQP5, and hyposecretion in the SHR SMGs

Objectives
Methods
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.