Abstract:
:Background Spontaneously hypertensive rats of the stroke-prone line (SHR-A3) develop hypertensive renal disease as a result of naturally occurring genetic variation. Our prior work identified a single-nucleotide polymorphism unique to SHR-A3 that results in truncation of the carboxy terminus of STIM1. The SHR-B2 line, which is also hypertensive but resists hypertensive renal injury, expresses the wild-type STIM1. STIM1 plays a central role in lymphocyte calcium signaling that directs immune effector responses. Here we show that major defects in lymphocyte function affecting calcium signaling, nuclear factor of activated T cells activation, cytokine production, proliferation, apoptosis, and regulatory T-cell development are present in SHR-A3 and attributable to STIM1. Methods and Results To assess the role of Stim1 variation in susceptibility to hypertensive renal injury, we created a Stim1 congenic line, SHR-A3(Stim1-B2), and STIM1 function was rescued in SHR-A3. We found that Stim1 gene rescue restores disturbed lymphocyte function in SHR-A3. Hypertensive renal injury was compared in SHR-A3 and the SHR-A3(Stim1-B2) congenic line. Histologically assessed renal injury was markedly reduced in SHR-A3(Stim1-B2), as were renal injury biomarker levels measured in urine. Stim1 deficiency has been linked to the emergence of antibody-mediated autoimmunity. Renal glomerular immunoglobulin deposition was greater in SHR-A3 than SHR-B2 and was reduced by Stim1 congenic substitution. Serum anti-double-stranded DNA antibody titers in SHR-A3 were elevated compared with SHR-B2 and were reduced in SHR-A3(Stim1-B2). Conclusions Stim1 deficiency in lymphocyte function originating from Stim1 truncation in SHR-A3 combines with hypertension to create end organ disease and may do so as a result of antibody formation.
journal_name
J Am Heart Assocjournal_title
Journal of the American Heart Associationauthors
Dhande IS,Zhu Y,Kneedler SC,Joshi AS,Hicks MJ,Wenderfer SE,Braun MC,Doris PAdoi
10.1161/JAHA.119.014142subject
Has Abstractpub_date
2020-03-03 00:00:00pages
e014142issue
5issn
2047-9980journal_volume
9pub_type
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journal_title:Journal of the American Heart Association
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doi:10.1161/JAHA.120.017835
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pub_type: 杂志文章
doi:10.1161/JAHA.117.007034
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pub_type: 杂志文章,实务指引,评审
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journal_title:Journal of the American Heart Association
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