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Research Article
Masao Toyoda
Tokai University
Corresponding Author
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The induction of a high blood pressure due to diabetic nephropathy depends on the increase in renin secretion from juxtaglomerular cells, but many aspects of how juxtaglomerular cells sense blood pressure changes in the afferent arteriole and consequently react remain unclear. In this study, we detected the juxtaglomerular cell-specific phosphorylation of the threonine-788/789 site of β1-integrin, and its expression was negatively correlated with renin production. This relationship was also observed in a culture system of a juxtaglomerular cell line, suggesting that β1-integrin is deeply involved in the regulation of renin production. The knockdown of β1-integrin in the culture system increased renin production, but the degree of the increase was comparable to the increase in renin production by knockdown of connexin-40, which is considered to be an important molecule that plays a role in the pressure sensing mechanism of juxtaglomerular cells. This suggests that the mechanism underlying the regulation of renin production by β1-integrin in juxtaglomerular cells may contribute to the pressure-sensing function of juxtaglomerular cells themselves. Threonine-788/789 phosphorylation of β1-integrin may be involved in the regulation of this pressoreceptor function.
(176 words)
Keywords
β1-integrin, diabetes, juxtaglomerular cells
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Competing interest reported. M.T. discloses the following relationships: honoraria from Kyowa Hakko Kirin, Chugai Pharmaceutical, Eli Lilly Japan K.K., MSD Corporation, Sumitomo Dainippon Pharma Co., Ltd.; grants from Sumitomo Dainippon Pharma Co., Ltd., Eli Lilly Japan K.K., LifeScan Japan, Kowa Company, Ltd., MSD Corporation, Sanwa Kagaku Kenkyusho. M.F. has acted as a consultant for Kyowa Hakko Kirin, Bayer Japan, and Novartis; has received honoraria from Kyowa Hakko Kirin, Chugai Pharmaceutical, Bayer Yakuhin, Novartis, Genzyme, and Abbot Japan; and has received grants/research support from Kyowa Hakko Kirin, Chugai Pharmaceutical, and Bayer Yakuhin. The other authors declare that they have no relevant financial or non-financial interests.
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research Article
Masao Toyoda
Tokai University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 25 Feb, 2021
No community comments so far
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Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
The induction of a high blood pressure due to diabetic nephropathy depends on the increase in renin secretion from juxtaglomerular cells, but many aspects of how juxtaglomerular cells sense blood pressure changes in the afferent arteriole and consequently react remain unclear. In this study, we detected the juxtaglomerular cell-specific phosphorylation of the threonine-788/789 site of β1-integrin, and its expression was negatively correlated with renin production. This relationship was also observed in a culture system of a juxtaglomerular cell line, suggesting that β1-integrin is deeply involved in the regulation of renin production. The knockdown of β1-integrin in the culture system increased renin production, but the degree of the increase was comparable to the increase in renin production by knockdown of connexin-40, which is considered to be an important molecule that plays a role in the pressure sensing mechanism of juxtaglomerular cells. This suggests that the mechanism underlying the regulation of renin production by β1-integrin in juxtaglomerular cells may contribute to the pressure-sensing function of juxtaglomerular cells themselves. Threonine-788/789 phosphorylation of β1-integrin may be involved in the regulation of this pressoreceptor function.
(176 words)
Figure 1
Figure 2
Figure 3
Figure 4
Competing interest reported. M.T. discloses the following relationships: honoraria from Kyowa Hakko Kirin, Chugai Pharmaceutical, Eli Lilly Japan K.K., MSD Corporation, Sumitomo Dainippon Pharma Co., Ltd.; grants from Sumitomo Dainippon Pharma Co., Ltd., Eli Lilly Japan K.K., LifeScan Japan, Kowa Company, Ltd., MSD Corporation, Sanwa Kagaku Kenkyusho. M.F. has acted as a consultant for Kyowa Hakko Kirin, Bayer Japan, and Novartis; has received honoraria from Kyowa Hakko Kirin, Chugai Pharmaceutical, Bayer Yakuhin, Novartis, Genzyme, and Abbot Japan; and has received grants/research support from Kyowa Hakko Kirin, Chugai Pharmaceutical, and Bayer Yakuhin. The other authors declare that they have no relevant financial or non-financial interests.
This is a list of supplementary files associated with this preprint. Click to download.
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