The functions of TRPP2 in the vascular system

Du, Juan; Fu, Jie; Shen, Bing

doi:10.1038/aps.2015.126

Cited by 19 publications

(20 citation statements)

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“…The transient receptor potential polycystic 2 (TRPP2, also known as polycystin-2, PC2, or PKD2) is a pivotal member of the mammalian transient receptor potential superfamily of channel proteins (5,27). TRPP2 is widely expressed in various tissues, including several types of smooth muscle cells, such as those in cerebral arteries, mesenteric arteries, the aorta, the gallbladder, and airway (6,7,22,24,29,34). The TRPP2 protein forms six transmembrane segments with an endoplasmic reticulum (ER) retention signal in the COOH-terminal domain and interacts with numerous proteins, mainly including cytoskeletal components (7,19).…”

Section: Introductionmentioning

confidence: 99%

“…TRPP2 is widely expressed in various tissues, including several types of smooth muscle cells, such as those in cerebral arteries, mesenteric arteries, the aorta, the gallbladder, and airway (6,7,22,24,29,34). The TRPP2 protein forms six transmembrane segments with an endoplasmic reticulum (ER) retention signal in the COOH-terminal domain and interacts with numerous proteins, mainly including cytoskeletal components (7,19). The TRPP2 channel protein, with a large single-channel conductance, as well as high Ca 2ϩ permeability, is encoded by the Pkd2 gene (7,19).…”

Section: Introductionmentioning

confidence: 99%

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Role of TRPP2 in mouse airway smooth muscle tension and respiration

Sang

Bai

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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The transient receptor potential polycystin-2 (TRPP2) is encoded by the Pkd2 gene, and mutation of this gene can cause autosomal dominant polycystic kidney disease (ADPKD). Some patients with ADPKD experience extrarenal manifestations, including radiologic and clinical bronchiectasis. We hypothesized that TRPP2 may regulate airway smooth muscle (ASM) tension. Thus, we used smooth muscle- Pkd2 conditional knockout ( Pkd2SM-CKO) mice to investigate whether TRPP2 regulated ASM tension and whether TRPP2 deficiency contributed to bronchiectasis associated with ADPKD. Compared with wild-type mice, Pkd2SM-CKO mice breathed more shallowly and faster, and their cross-sectional area ratio of bronchi to accompanying pulmonary arteries was higher, suggesting that TRPP2 may regulate ASM tension and contribute to the occurrence of bronchiectasis in ADPKD. In a bioassay examining isolated tracheal ring tension, no significant difference was found for high-potassium-induced depolarization of the ASM between the two groups, indicating that TRPP2 does not regulate depolarization-induced ASM contraction. By contrast, carbachol-induced contraction of the ASM derived from Pkd2SM-CKO mice was significantly reduced compared with that in wild-type mice. In addition, relaxation of the carbachol-precontracted ASM by isoprenaline, a β-adrenergic receptor agonist that acts through the cAMP/adenylyl cyclase pathway, was also significantly attenuated in Pkd2SM-CKO mice compared with that in wild-type mice. Thus, TRPP2 deficiency suppressed both contraction and relaxation of the ASM. These results provide a potential target for regulating ASM tension and for developing therapeutic alternatives for some ADPKD complications of the respiratory system or for independent respiratory disease, especially bronchiectasis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of TRPP2 in mouse airway smooth muscle tension and respiration

Sang

Bai

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The PKD2 gene extends over 70 kb of the genome and contains 15 exons that produce a 3 kb mRNA [ 11 ]. Its encoding product, polycystin-2, consists of 968 amino acids, which form six transmembrane domains [ 12 ]. Polycystin-2 interacts with polycystin-1 through its C-terminal domain, and this interaction is considered to be indispensable for fluid-flow sensation by the primary cilium of renal epithelial cells [ 8 ].…”

Section: Discussionmentioning

confidence: 99%

Whole exome sequencing reveals a stop-gain mutation of PKD2 in an autosomal dominant polycystic kidney disease family complicated with aortic dissection

et al. 2018

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BackgroundAutosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disorder characterized by progressive cyst formation and expansion in the kidneys, which culminates in end-stage renal disease. Aortic dissection is a rare vascular complication of ADPKD and related literature is currently limited.Case presentationIn this report, we described a patient with asymptomatic Stanford B aortic dissection. Further investigation revealed a positive family history of ADPKD and normal renal function. Whole exome sequencing identified a stop-gain mutation c.1774C > T, p.Arg592Ter in the PKD2 gene that segregated in the family. To our knowledge, this is the first report of ADPKD complicated with aortic dissection caused by PKD2 mutation.ConclusionsThe case illustrates the importance of aorta imaging and molecular diagnosis in ADPKD patients in order to achieve early recognition of the deadly vascular complication.

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“…TRPP channels consist of TRPP1, TRPP2, and TRPP3. Among TRPP family, TRPP1 can interact with Polycystin-1 [ 60 ]; TRPP2 along with Polycystin-1, TRPV4, and TRPC1, then functioning as mechanosensitive channels [ 61 ]. TRPP1 and TRPP2 are both expressed in vascular smooth muscle and EC from cerebral and mesenteric arteries playing a role in regulation of blood vessel function and myogenic tone [ 130 , 131 ].…”

Section: Trp Channelsmentioning

confidence: 99%

Mechanosensitivity in Pulmonary Circulation: Pathophysiological Relevance of Stretch-Activated Channels in Pulmonary Hypertension

et al. 2021

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A variety of cell types in pulmonary arteries (endothelial cells, fibroblasts, and smooth muscle cells) are continuously exposed to mechanical stimulations such as shear stress and pulsatile blood pressure, which are altered under conditions of pulmonary hypertension (PH). Most functions of such vascular cells (e.g., contraction, migration, proliferation, production of extracellular matrix proteins, etc.) depend on a key event, i.e., the increase in intracellular calcium concentration ([Ca2+]i) which results from an influx of extracellular Ca2+ and/or a release of intracellular stored Ca2+. Calcium entry from the extracellular space is a major step in the elevation of [Ca2+]i, involving a variety of plasmalemmal Ca2+ channels including the superfamily of stretch-activated channels (SAC). A common characteristic of SAC is that their gating depends on membrane stretch. In general, SAC are non-selective Ca2+-permeable cation channels, including proteins of the TRP (Transient Receptor Potential) and Piezo channel superfamily. As membrane mechano-transducers, SAC convert physical forces into biological signals and hence into a cell response. Consequently, SAC play a major role in pulmonary arterial calcium homeostasis and, thus, appear as potential novel drug targets for a better management of PH.

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The functions of TRPP2 in the vascular system

Cited by 19 publications

References 84 publications

Role of TRPP2 in mouse airway smooth muscle tension and respiration

Role of TRPP2 in mouse airway smooth muscle tension and respiration

Whole exome sequencing reveals a stop-gain mutation of PKD2 in an autosomal dominant polycystic kidney disease family complicated with aortic dissection

Mechanosensitivity in Pulmonary Circulation: Pathophysiological Relevance of Stretch-Activated Channels in Pulmonary Hypertension

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