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We hypothesize that microR\u2010210 plays a protective role explaining this difference. Both male and female adults with T1D and T2D matched for glycated hemoglobin, alongside age\u2010 and sex\u2010matched healthy controls, were studied. microR\u2010210 levels were measured by qPCR. Endothelium\u2010dependent relaxation (EDR) in isolated rat aortas and nitric oxide (NO) production in endothelial cells following incubation with RBCs were determined using wire myograph and DAF\u2010FM fluorescence. Protein levels of microR\u2010210 target PTP1B and the oxidative stress marker 4\u2010HNE were measured by immunohistochemistry. T1D RBC produced EDR and endothelial NO comparable to healthy controls, whereas T2D RBC impaired both. microR\u2010210 levels were similar in T1D RBC and healthy controls, but reduced in T2D RBC. microR\u2010210 inhibition in T1D RBC impaired EDR and increased vascular PTP1B and 4\u2010HNE, while PTP1B inhibition or mitoTEMPO treatment in aortas improved EDR. 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