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Orai1 downregulation impairs lymphocyte function in type 2 diabetes mellitus
Haoyang Wang1, Cong Wang1, Limin Wang1
1Department of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Biochemical and Biophysical Research Communications
|April 15, 2018
Summary
Diabetes impairs T lymphocyte function by reducing calcium (Ca2+) signaling. This study found decreased Ca2+ influx and Orai1 protein expression in diabetic T cells, revealing a key mechanism for immune dysfunction.
Area of Science:
- Immunology
- Cell Biology
- Diabetology
Background:
- Diabetes mellitus is linked to immune dysfunction, with potential calcium (Ca2+) signaling defects in lymphocytes.
- The precise mechanisms underlying Ca2+ signal dysregulation in diabetic lymphocytes remain unclear.
Purpose of the Study:
- To investigate alterations in intracellular Ca2+ signals in T lymphocytes from diabetic individuals.
- To elucidate the underlying mechanisms contributing to T lymphocyte malfunction in diabetes.
Main Methods:
- Calcium influx was measured using Fura-2-AM in T lymphocytes from diabetic patients and animals.
- Orai1 protein and mRNA expression were analyzed via Western blot and qRT-PCR.
- Jurkat T cells were treated with high glucose and agonists to assess Ca2+ entry and IL-2 release.
Main Results:
- A significant decrease in Ca2+ influx was observed in T lymphocytes from diabetic sources.
- Downregulated Orai1 protein expression, but not mRNA, was found in these cells.
- High glucose and agonist treatment reduced Ca2+ entry and IL-2 release in Jurkat cells, correlating with decreased Orai1 expression.
Conclusions:
- Declined Orai1 expression contributes to reduced Ca2+ entry in T lymphocytes during stimulation.
- This Orai1-mediated mechanism offers insight into T lymphocyte malfunction observed in diabetes.
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