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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Am+Soc+Nephrol
2016 ; 27
(4
): 1135-44
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Phosphoinositide 3-Kinase-C2? Regulates Polycystin-2 Ciliary Entry and Protects
against Kidney Cyst Formation
#MMPMID26271513
Franco I
; Margaria JP
; De Santis MC
; Ranghino A
; Monteyne D
; Chiaravalli M
; Pema M
; Campa CC
; Ratto E
; Gulluni F
; Perez-Morga D
; Somlo S
; Merlo GR
; Boletta A
; Hirsch E
J Am Soc Nephrol
2016[Apr]; 27
(4
): 1135-44
PMID26271513
show ga
Signaling from the primary cilium regulates kidney tubule development and cyst
formation. However, the mechanism controlling targeting of ciliary components
necessary for cilium morphogenesis and signaling is largely unknown. Here, we
studied the function of class II phosphoinositide 3-kinase-C2? (PI3K-C2?) in
renal tubule-derived inner medullary collecting duct 3 cells and show that
PI3K-C2? resides at the recycling endosome compartment in proximity to the
primary cilium base. In this subcellular location, PI3K-C2? controlled the
activation of Rab8, a key mediator of cargo protein targeting to the primary
cilium. Consistently, partial reduction of PI3K-C2? was sufficient to impair
elongation of the cilium and the ciliary transport of polycystin-2, as well as to
alter proliferation signals linked to polycystin activity. In agreement,
heterozygous deletion of PI3K-C2? in mice induced cilium elongation defects in
kidney tubules and predisposed animals to cyst development, either in genetic
models of polycystin-1/2 reduction or in response to ischemia/reperfusion-induced
renal damage. These results indicate that PI3K-C2? is required for the transport
of ciliary components such as polycystin-2, and partial loss of this enzyme is
sufficient to exacerbate the pathogenesis of cystic kidney disease.
|*Kidney Diseases, Cystic/etiology
[MESH]
|Animals
[MESH]
|Cilia/*physiology
[MESH]
|Class II Phosphatidylinositol 3-Kinases/*physiology
[MESH]
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