Upper urinary tract pacemaker cells join the GLI club

Herzlinger, Doris

doi:10.1172/jci46400

Cited by 11 publications

(4 citation statements)

References 15 publications

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“…Although the urothelium and SMCs develop normally in these mutant mice, the number of ureteral pacemaker cells (marked by Kit and Hcn3 expression) in the renal pelvis and the ureter are significantly reduced 76. This study provides strong evidence that sonic hedgehog signaling controls ureteral pacemaker cell development and defective pacemaker cell differentiation can lead to abnormal ureteral peristalsis and hydronephrosis 76,262. Consistent with this finding, mutations in the GLI3 gene have been identified in patients with the Pallister–Hall syndrome (PHS, OMIM: 146510), which includes urinary tract phenotypes like hydronephrosis and hydroureter 263–265…”

Section: Genetic Basis Of Calutsupporting

confidence: 70%

Performance analysis of cooperative multi‐carrier relay‐based UAV networks over generalized fading channels

Abualhaol

Matalgah

2011

Int J Communication

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SUMMARYThe outage probability in a network of cooperative unmanned airborne vehicles (UAVs) over generalized fading channels is studied analytically using finite mixture with expectation maximization technique. A relay-based topology with one ground control unit (GCU) is considered, where the cooperative UAVs can communicate with the GCU directly or through relay. The application the UAV is assigned for specifies the minimum required transmission rate the UAV should achieve. The outage probability of the system is defined as the probability that either the transmission rate over any of the links drops below a predefined minimum threshold for that link or the Relay-GCU link is not able to transmit the aggregate data from all relayed UAVs and the minimum rate required by the relay UAV itself. Throughout the paper, expressions for the outage probability and the average achievable bit rate of a cooperative multicarrier system are derived over generalized fading channels. Finite mixture with expectation maximization algorithm is utilized to derive a simple approximate expression for the probability density function (pdf) of the achievable bit rate assuming adaptive M-ary quadrature amplitude modulation (M-QAM). This pdf is used to derive closed-form expressions for the outage probability and the average bit rate.

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Section: Genetic Basis Of Calutsupporting

confidence: 70%

Performance analysis of cooperative multi‐carrier relay‐based UAV networks over generalized fading channels

Abualhaol

Matalgah

2011

Int J Communication

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“…76 This study provides strong evidence that sonic hedgehog signaling controls ureteral pacemaker cell development and defective pacemaker cell differentiation can lead to abnormal ureteral peristalsis and hydronephrosis. 76,262 Consistent with this finding, mutations in the GLI3 gene have been identified in patients with the Pallister-Hall syndrome (PHS, OMIM: 146510), which includes urinary tract phenotypes like hydronephrosis and hydroureter. [263][264][265] In another study, Chang et al have shown that expression of one of the calcineurin subunit B isoform genes Cnb1 (also called Ppp3r1) is required in the mouse urinary tract mesenchyme for the development of the pyeloureteral peristaltic machinery.…”

Section: Mutations In Genes Controlling Ureter Developmentmentioning

confidence: 67%

Lower urinary tract development and disease

Rasouly

2013

WIREs Mechanisms of Disease

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Congenital Anomalies of the Lower Urinary Tract (CALUT) are a family of birth defects of the ureter, the bladder and the urethra. CALUT includes ureteral anomalies such as congenital abnormalities of the ureteropelvic junction (UPJ) and ureterovesical junction (UVJ), and birth defects of the bladder and the urethra such as bladder-exstrophy-epispadias complex (BEEC), prune belly syndrome (PBS), and posterior urethral valves (PUV). CALUT is one of the most common birth defects and is often associated with antenatal hydronephrosis, vesicoureteral reflux (VUR), urinary tract obstruction, urinary tract infections (UTI), chronic kidney disease and renal failure in children. Here, we discuss the current genetic and molecular knowledge about lower urinary tract development and genetic basis of CALUT in both human and mouse models. We provide an overview of the developmental processes leading to the formation of the ureter, bladder, and urethra, and different genes and signaling pathways controlling these developmental processes. Human genetic disorders that affect the ureter, bladder and urethra and associated gene mutations are also presented. As we are entering the post-genomic era of personalized medicine, information in this article may provide useful interpretation for the genetic and genomic test results collected from patients with lower urinary tract birth defects. With evidence-based interpretations, clinicians may provide more effective personalized therapies to patients and genetic counseling for their families.

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“…2005; Cain et al . 2011; Herzlinger, 2011). In this study, we discovered that c‐Kit + /CD45 − ICs (KICs) are a minor population of cells in the renal pelvis, and the majority of c‐Kit + cells are mast cells.…”

Section: Discussionmentioning

confidence: 99%

Identification and classification of interstitial cells in the mouse renal pelvis

Grainger

Freeman

Shonnard

et al. 2020

The Journal of Physiology

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Platelet-derived growth factor receptor-α (PDGFRα) is a novel biomarker along with smooth myosin heavy chain for the pacemaker cells (previously termed 'atypical' smooth muscle cells) in the murine and cynomolgus monkey pelvis-kidney junction. r PDGFRα + cells present in adventitial and urothelial layers of murine renal pelvis do not express smooth muscle myosin heavy chain (smMHC) but are in close apposition to nerve fibres. r Most c-Kit + cells in the renal pelvis are mast cells. Mast cells (CD117 + /CD45 +) are more abundant in the proximal renal pelvis and pelvis-kidney junction regions whereas c-Kit + interstitial cells (CD117 + /CD45 −) are found predominantly in the distal renal pelvis and ureteropelvic junction. r PDGFRα + cells are distinct from c-Kit + interstitial cells. r A subset of PDGFRα + cells express the Ca 2+-activated Cl − channel, anoctamin-1, across the entire renal pelvis. r Spontaneous Ca 2+ transients were observed in c-Kit + interstitial cells, smMHC + PDGFRα cells and smMHC − PDGFRα cells using mice expressing genetically encoded Ca 2+ sensors.

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Upper urinary tract pacemaker cells join the GLI club

Cited by 11 publications

References 15 publications

Performance analysis of cooperative multi‐carrier relay‐based UAV networks over generalized fading channels

Performance analysis of cooperative multi‐carrier relay‐based UAV networks over generalized fading channels

Lower urinary tract development and disease

Identification and classification of interstitial cells in the mouse renal pelvis

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