The kinin receptor is expressed in the Malpighian tubule stellate cells in the mosquito Aedes aegypti (L.): A new model needed to explain ion transport?

Abstract

It is known that insect kinins increase diuresis and fluid secretion in the Aedes aegypti Malpighian tubule, causing a rapid drop of the transepithelial resistance and increasing chloride conductance from the hemolymph towards the tubule lumen. The tubule is composed of both principal and stellate cells. The main route for increased chloride influx upon kinin treatment is proposed to be paracellular, with septate junctions acquiring increased chloride selectivity and conductance. Therefore, kinin treatment renders the Aedes aegypti tubule a "leaky epithelium", and under this model the kinin receptor is postulated to be expressed in principal cells. However, in another dipteran, the fruit fly Drosophila melanogaster, the main route for chloride transport is transcellular through stellate cells. In both the fruit fly and the mosquito Anopheles stephensi the kinin receptor has been immunolocalized in stellate cells, where it regulates transepithelial chloride permeability. Here we show that in Aedes aegypti, similarly, the stellate cells express the kinin receptor. This was confirmed through immunohistochemistry with two specific anti-kinin receptor antibodies and confocal analysis. The receptor is detected as a 75kDa band in western blot. These results indicate that the currently accepted model for chloride transport must be reevaluated in Aedes aegypti and suggest the kinin regulatory signals controlling intercellular junctions originate in the stellate cells.

Cloning and functional characterization of inward-rectifying potassium (Kir) channels from Malpighian tubules of the mosquito Aedes aegypti

“…Kinins, such as leucokinins and aedeskinins, impart their diuretic effects on Malpighian tubules by binding to a G protein-coupled receptor on stellate and principal cells (Lu et al, 2011; Yu and Beyenbach, 2004), which leads to a rise of intracellular Ca2 + (Yu and Beyenbach, 2002). Calcium then stimulates the transepithelial secretion of NaCl, KCl, and water by signaling to the paracellular pathway and apical V-type H + -ATPase (Beyenbach et al, 2009).…”

Leucokinin mimetic elicits aversive behavior in mosquito Aedes aegypti (L.) and inhibits the sugar taste neuron

“…5. Details of mosquito rearing, kinin analogs, no-choice feeding assays with kinin analogs, frozen-section immunohistochemistry of Aedae-KR in labellum and prothoracic tarsi, electrophysiological recordings on labellar long hair sensilla, the effects of gene silencing on feeding behavior, dsRNA synthesis and the efficiency of knockdown, and statistical analyses are provided in SI Materials and Methods.…”

“…Neuropeptide diuretic hormones increase the secretion of primary urine by the Malpighian tubules and increase hindgut contractions, which aid in fluid excretion (4). In A. aegypti, three endogenous kinins (aedeskinin I-III) act as diuretic hormones on Malpighian tubule stellate cells (5,6) by stimulating chloride transport and fluid secretion (6)(7)(8). We verified that the aedeskinins activate the single Aedes kinin receptor (Aedae-KR), a G protein-coupled receptor (GPCR) that signals through intracellular calcium (9).…”

Role in Diuresis of a Calcitonin Receptor (GPRCAL1) Expressed in a Distal-Proximal Gradient in Renal Organs of the Mosquito Aedes aegypti (L.)

“…These act on cognate receptors in the renal organs, the Malpighian tubules (MTs), to stimulate ion transport for primary urine production and subsequent fluid excretion. In hematophagous female mosquitoes excess fluid and ions (Na + , Cl − , K + ) acquired with the blood meal are transported from the hemolymph to the MT lumen to secrete urine at extremely high rate [5], [6]. Transport is achieved by channels and co-transporters in the MT principal and stellate cells and through septate junctions between principal cells and is energized by an apical vacuolar H + -ATPase (V-ATPase) in the principal cells.…”