Microvesicles (or MVs) are plasma membrane-derived vesicles released from most eukaryotic cells constitutively during early apoptosis or at higher levels after chemical or physical stress conditions. This review looks at some of the functions of MVs in terms of intercellular communication and ensuant signal transduction, including the transport of proteins (unconventional protein export) as well as of mRNA and microRNA. MVs also have roles in membrane repair, the removal of misfolded proteins, and in the control of apoptosis. We also discuss the role MVs have been shown to have in invasive growth and metastasis as well as in hypoxia in tumours and cerebral ischaemia. The association of MVs in infectious and autoimmune disease is also summarised together with their possible use as therapeutic agents.

Anemia is defined as a reduction in the hemoglobin concentration of blood, which consequently reduces the oxygen-carrying capacity of red blood cells such that they are unable to meet the body’s physiological needs. Several reports have indicated that anemia mostly occurs in patients with diabetes with renal insufficiency while limited studies have reported the incidence of anemia in people with diabetes prior to evidence of renal impairment. Other studies have also identified anemia as a risk factor for the need for renal replacement therapy in diabetes. Understanding the pathogenesis of anemia associated with diabetes may lead to the development of interventions to optimize outcomes in these patients. The aim of this study was therefore to determine the prevalence of anemia among patients with type 2 diabetes. A total of 100 (50 with type 2 diabetes and 50 controls) participants were recruited for our study. Participants’ blood samples were analyzed for fasting blood glucose, full blood count and renal function tests among others. The prevalence of anemia was then determined statistically. A high incidence of anemia was observed in the cases. Of the patients with diabetes, 84.8 % had a hemoglobin concentration that was significantly less (males 11.16±1.83 and females 10.41±1.49) than the controls (males 14.25±1.78 and females 12.53±1.14). Renal insufficiency determined by serum creatinine level of >1.5 mg/dL, estimated glomerular filtration rate <60 ml/minute/1.73 m2, and erythropoietin levels was also observed to be high in the cases (54.0 %; with mean creatinine concentration of 3.43±1.73 and erythropoietin 6.35±1.28 mIU/mL). A significantly increased fasting blood glucose, urea, sodium, potassium, and calcium ions were observed in the cases (7.99±1.30, 5.19±1.99, 140.90±6.98, 4.86±0.53 and 1.47±0.31 respectively) as compared to the controls (4.66±0.54, 3.56±2.11, 135.51±6.84, 4.40±0.58 and 1.28±0.26 respectively). Finally, a significant association between hemoglobin concentration and fasting blood glucose was also observed in the cases. The findings suggest that a high incidence of anemia is likely to occur in patients with poorly controlled diabetes and in patients with diabetes and renal insufficiency.

Plasma membrane-derived vesicles (PMVs) are small intact vesicles released from the cell surface that play a role in intercellular communication. We have examined the role of PMVs in the terminal differentiation of monocytes. The myeloid-differentiating agents all-trans retinoic acid/PMA and histamine, the inflammatory mediator that inhibits promonocyte proliferation, induced an intracellular Ca²⁺-mediated PMV (as opposed to exosome) release from THP-1 promonocytes. These PMVs cause THP-1 cells to enter G₀–G₁ cell cycle arrest and induce terminal monocyte-to-macrophage differentiation. Use of the TGF-β receptor antagonist SB-431542 and anti–TGF-β1 Ab showed that this was due to TGF-β1 carried on PMVs. Although TGF-β1 levels have been shown to increase in cell culture supernatants during macrophage differentiation and dendritic cell maturation, the presence of TGF-β1 in PMVs is yet to be reported. In this study, to our knowledge we show for the first time that TGF-β1 is carried on the surface of PMVs, and we confirm the presence within PMVs of certain leaderless proteins, with reported roles in myeloid cell differentiation. Our in vitro findings support a model in which TGF-β1–bearing PMVs, released from promonocytic leukemia cells (THP-1) or primary peripheral blood monocytes on exposure to sublytic complement or after treatment with a differentiation therapy agent, such as all-trans retinoic acid, significantly reduce proliferation of THP-1 cells. Such PMVs also induce the terminal differentiation of primary peripheral blood monocytes as well as THP-1 monocytes.