Type 2 diabetes mellitus stimulated pulmonary vascular inflammation and exosome biogenesis in rats

It has been shown that type 2 Diabetes Mellitus (T2DM) changes the paracrine
activity of several cell types. Whether the biogenesis of exosomes is changed during
diabetic conditions is the subject of debate. Here, we investigated the effect of T2M
on exosome biogenesis in rat pulmonary tissue. Rats received a high‐fat diet regime
and a single low dose of Streptozocin to mimic the T2DM‐like condition. A total of
8 weeks after induction of T2DM, rats were subjected to several analyses. Besides
histological examination, vascular cell adhesion molecule 1 (VCAM‐1) levels were
detected using immunohistochemistry (IHC) staining. Transcription of several genes
such as IL‐1β, Alix, and Rab27b was calculated by real‐time polymerase chain
reaction assay. Using western blot analysis, intracellular CD63 levels were measured.
The morphology and exosome secretion activity were assessed using acetylcholinesterase
(AChE) assay and scanning electron microscopy, respectively. Histological
results exhibited a moderate‐to‐high rate of interstitial pneumonia with emphysematous
changes. IHC staining showed an increased VCAM‐1 expression in the
diabetic lungs compared with the normal conditions (p < .05). Likewise, we found the
induction of IL‐1β, and exosome‐related genes Alix and Rab27b under diabetic
conditions compared with the control group (p < .05). Along with these changes,
protein levels of CD63 and AChE activity were induced upon the initiation of T2DM,
indicating accelerated exosome biogenesis. Taken together, current data indicated
the induction of exosome biogenesis in rat pulmonary tissue affected by T2DM. It
seems that the induction of inflammatory niche is touted as a stimulatory factor to
accelerate exosome secretion.