Removal of the MDCK Cell Primary Cilium Abolishes Flow Sensing

Praetorius, Helle A.; Spring, Kenneth R.

doi:10.1007/s00232-002-1042-4

Cited by 314 publications

(264 citation statements)

References 13 publications

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“…Such a function could be fluid flow sensing [54]. In support of this hypothesis, it has been shown that mechanical bending of the primary cilium or fluid flow in MDCK cells resulted in increases in intracellular Ca 2+ concentration which was dependent on extracellular Ca 2+ , PLC activation and inositol 1,4,5 trisphosphate (IP 3 )-induced release of intracellular Ca 2+ stores [55][56][57]. It is noteworthy that bending-induced Ca 2+ signaling was not affected by inhibition of ryonodine receptors [55].…”

Section: Function At the Primary Ciliummentioning

confidence: 91%

Cell biology of polycystin-2

Tsiokas¹,

Kim²,

Ong³

2007

Cellular Signalling

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Naturally occurring mutations in two separate, but interacting loci, pkd1 and pkd2 are responsible for almost all cases of autosomal dominant polycystic kidney disease (ADPKD). ADPKD is one of the most common genetic diseases resulting primarily in the formation of large kidney, liver, and pancreatic cysts. Homozygous deletion of either pkd1 or pkd2 results in embryonic lethality in mice due to kidney and heart defects illustrating their indispensable roles in mammalian development. However, the mechanism by which mutations in these genes cause ADPKD and other developmental defects are unknown. Research in the past several years has revealed that PKD2 has multiple functions depending on its subcellular localization. It forms a receptor-operated, non-selective cation channel in the plasma membrane, a novel intracellular Ca 2+ release channel in the endoplasmic reticulum (ER), and a mechanosensitive channel in the primary cilium. This review focuses on the functional compartmentalization of PKD2, its modes of activation, and PKD2-mediated signal transduction.

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Section: Function At the Primary Ciliummentioning

confidence: 91%

Cell biology of polycystin-2

Tsiokas¹,

Kim²,

Ong³

2007

Cellular Signalling

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“…In mice lacking P2X 4 receptors, flowinduced increases of [Ca 2+ ] i in the endothelial cells were absent, as was the endothelium-dependent vascular dilatation. Flow-induced increases in [Ca 2+ ] i can also be elicited in renal epithelia [130][131][132]. This phenomenon has received much attention as it was hypothesised that an absence of flow sensing in renal epithelia causes polycystic kidney disease [133].…”

Section: Mechanically Released Nucleotidesmentioning

confidence: 99%

ATP release from non-excitable cells

Praetorius

Leipziger

2009

Purinergic Signalling

207

229

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All cells release nucleotides and are in one way or another involved in local autocrine and paracrine regulation of organ function via stimulation of purinergic receptors. Significant technical advances have been made in recent years to quantify more precisely resting and stimulated adenosine triphosphate (ATP) concentrations in close proximity to the plasma membrane. These technical advances are reviewed here. However, the mechanisms by which cells release ATP continue to be enigmatic. The current state of knowledge on different suggested mechanisms is also reviewed. Current evidence suggests that two separate regulated modes of ATP release co-exist in nonexcitable cells: (1) a conductive pore which in several systems has been found to be the channel pannexin 1 and (2) vesicular release. Modes of stimulation of ATP release are reviewed and indicate that both subtle mechanical stimulation and agonist-triggered release play pivotal roles. The mechano-sensor for ATP release is not yet defined.

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“…Primary cilia were removed from CHEC essentially as was described before (Praetorius and Spring, 2003). In short, CHEC were treated for 72 hr with 5ϫ10 -3 Mol/L Chloral Hydrate (Sigma) in tissue culture medium to remove cilia, followed by 24 hr recovery in standard medium.…”

Section: Removal Of Endothelial Cilia In Vitromentioning

confidence: 99%

Primary cilia sensitize endothelial cells for fluid shear stress

Hierck

Heiden

Alkemade

et al. 2008

Developmental Dynamics

159

108

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Primary cilia are mechanosensors for fluid shear stress, and are involved in a number of syndromes and congenital anomalies. We identified endothelial cilia in areas of low shear stress in the embryonic heart. The objective of the present study was to demonstrate the role of primary cilia in mechanosensing. Ciliated embryonic endothelial cells were cultured from the heart, and non-ciliated cells from the arteries. Nonciliated cells that were subjected to fluid shear stress showed significantly less induction of the shear marker Krü ppel-Like Factor-2, as compared to ciliated cells. In addition, ciliated cells from which the cilia were chemically removed show a similar decrease in flow response. This shows that primary cilia sensitize endothelial cells for fluid shear stress. In addition, we targeted and stabilized the connection of the cilium to the cytoplasm by treatment with Colchicine and Taxol/Paclitaxel, respectively, and show that microtubular integrity is essential to sense shear stress. Developmental Dynamics 237:725-735, 2008.

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Removal of the MDCK Cell Primary Cilium Abolishes Flow Sensing

Cited by 314 publications

References 13 publications

Cell biology of polycystin-2

Cell biology of polycystin-2

ATP release from non-excitable cells

Primary cilia sensitize endothelial cells for fluid shear stress

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