Insulin-like growth factor-II: a novel autocrine growth factor modulating the apoptosis and maturation of umbilical cord blood erythroid progenitors

Nagatomo, Taro; Muta, Koichiro; Ohga, Shouichi; Ochiai, Masayuki; Ohshima, Koichi; Hara, Toshiro

doi:10.1016/j.exphem.2007.12.009

Cited by 2 publications

(1 citation statement)

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“…Our finding during the current study that granulocytes and oenocytoids express the MIR is also consistent with the suggestion that mosquito hemocytes proliferate in direct response to ILP3. The ILP bombyxin has likewise been implicated in stimulating hemocyte proliferation in the silkmoth, Bombyx mori [39], while studies with mammals implicate insulin growth factor-like signaling in proliferation of lymphocytes [40]–[42]. A recent study also implicates a cell surface protein designated crustacean hematopoietic factor (CHF) in survival of certain hemocyte types from the crayfish Pacifastacus leniusculus [43].…”

Section: Discussionmentioning

confidence: 99%

Blood Feeding and Insulin-like Peptide 3 Stimulate Proliferation of Hemocytes in the Mosquito Aedes aegypti

2011

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All vector mosquito species must feed on the blood of a vertebrate host to produce eggs. Multiple cycles of blood feeding also promote frequent contacts with hosts, which enhance the risk of exposure to infectious agents and disease transmission. Blood feeding triggers the release of insulin-like peptides (ILPs) from the brain of the mosquito Aedes aegypti, which regulate blood meal digestion and egg formation. In turn, hemocytes serve as the most important constitutive defense in mosquitoes against pathogens that enter the hemocoel. Prior studies indicated that blood feeding stimulates hemocytes to increase in abundance, but how this increase in abundance is regulated is unknown. Here, we determined that phagocytic granulocytes and oenocytoids express the A. aegypti insulin receptor (AaMIR). We then showed that: 1) decapitation of mosquitoes after blood feeding inhibited hemocyte proliferation, 2) a single dose of insulin-like peptide 3 (ILP3) sufficient to stimulate egg production rescued proliferation, and 3) knockdown of the AaMIR inhibited ILP3 rescue activity. Infection studies indicated that increased hemocyte abundance enhanced clearance of the bacterium Escherichia coli at lower levels of infection. Surprisingly, however, non-blood fed females better survived intermediate and high levels of E. coli infection than blood fed females. Taken together, our results reveal a previously unrecognized role for the insulin signaling pathway in regulating hemocyte proliferation. Our results also indicate that blood feeding enhances resistance to E. coli at lower levels of infection but reduces tolerance at higher levels of infection.

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