Cyclophosphamide Induced Cystitis Alters Neurotrophin and Receptor Tyrosine Kinase Expression in Pelvic Ganglia and Bladder

Murray, Elaine; Malley, Susan E.; Qiao, Li‐Ya; Hu, Vivian Y.; Vizzard, Margaret A.

doi:10.1097/01.ju.0000143549.29867.4e

Cited by 87 publications

(101 citation statements)

References 21 publications

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“…As previously described (Vizzard, 2000c;Murray et al, 2004), tissue was homogenized and centrifuged (10,000 rpm for 5 min); supernatants were used for NGF quantification. Total protein was determined (Pierce).…”

Section: Enzyme-linked Immunoassays For Ngf In Urinary Bladdermentioning

confidence: 99%

Expression of Phosphorylated cAMP Response Element Binding Protein (p-CREB) in Bladder Afferent Pathways in VIP−/− Mice with Cyclophosphamide (CYP)-Induced Cystitis

et al. 2008

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The expression of phosphorylated cAMP response element binding protein (pCREB) in dorsal root ganglia (DRG) with and without CYP-induced cystitis (150 mg/kg, i.p; 48 hr) was determined in VIP −/− and wildtype (WT) mice. p-CREB-immunoreactivity (IR) was determined in bladder (Fastblue) afferent cells. Nerve growth factor (NGF) bladder content was determined by ELISAs. Basal expression of pCREB-IR in DRG of VIP −/− mice was (p ≤ 0.01) greater in L1, L2, L5-S1 DRG compared to WT mice. CYP treatment in WT mice increased (p ≤ 0.05) pCREB-IR in L1, L2, L5-S1 DRG. CYP treatment in VIP −/− mice (p ≤ 0.01) increased (p ≤ 0.01) p-CREB-IR in L6-S1 DRG compared to WT with CYP. In WT mice, bladder afferent cells (20-38%) in DRG expressed pCREB-IR under basal conditions. With CYP, pCREB-IR increased in bladder afferent cells (60-65%; L6-S1 DRG) in WT mice. In VIP −/− mice, bladder afferent cells (12-58%) expressed pCREB-IR under basal conditions and CYP increased pCREB expression (78-84%) in L6-S1 DRG. Urinary bladder NGF expression in VIP −/− mice under basal conditions or after cystitis was significantly greater than WT. Detrusor smooth muscle thickness was significantly increased in VIP −/− mice. Bladder NGF expression may contribute to differences in pCREB expression.

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Section: Enzyme-linked Immunoassays For Ngf In Urinary Bladdermentioning

confidence: 99%

Expression of Phosphorylated cAMP Response Element Binding Protein (p-CREB) in Bladder Afferent Pathways in VIP−/− Mice with Cyclophosphamide (CYP)-Induced Cystitis

et al. 2008

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“…A possible explanation relies on the following observations: (1) Although in the neuronal system, high concentrations of mature NTs required to induce even modest levels of apoptosis are considered non-physiological, 34 in human epidermis, the NT-4, BDNF or other yet unidentified ligands could autocrinally and paracrinally be continuously released and in turn bind p75NTR, thus overcoming Trk functions. (2) Epithelial cells behave differently from neurons, as normal prostate and bladder cells express Trk 35,36 and still undergo apoptosis via p75NTR binding. 37 It has been recently shown that, under certain circumstances and stimuli, a Trk-to-p75NTR molecular switch occurs favoring cell death.…”

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confidence: 99%

p75 neurotrophin receptor mediates apoptosis in transit-amplifying cells and its overexpression restores cell death in psoriatic keratinocytes

et al. 2010

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p75 neurotrophin receptor (p75NTR) belongs to the TNF-receptor superfamily and signals apoptosis in many cell settings. In human epidermis, p75NTR is mostly confined to the transit-amplifying (TA) sub-population of basal keratinocytes. Brainderived neurotrophic factor (BDNF) or neurotrophin-4 (NT-4), which signals through p75NTR, induces keratinocyte apoptosis, whereas b-amyloid, a ligand for p75NTR, triggers caspase-3 activation to a greater extent in p75NTR transfected cells. Moreover, p75NTR co-immunoprecipitates with NRAGE, induces the phosphorylation of c-Jun N-terminal kinase (JNK) and reduces nuclear factor kappa B (NF-jB) DNA-binding activity. p75NTR also mediates pro-NGF-induced keratinocyte apoptosis through its co-receptor sortilin. Furthermore, BDNF or b-amyloid cause cell death in TA, but not in keratinocyte stem cells (KSCs) or in p75NTR silenced TA cells. p75NTR is absent in lesional psoriatic skin and p75NTR levels are significantly lower in psoriatic than in normal TA keratinocytes. The rate of apoptosis in psoriatic TA cells is significantly lower than in normal TA cells. BDNF or b-amyloid fail to induce apoptosis in psoriatic TA cells, and p75NTR retroviral infection restores BDNF-or b-amyloid-induced apoptosis in psoriatic keratinocytes. These results demonstrate that p75NTR has a pro-apoptotic role in keratinocytes and is involved in the maintenance of epidermal homeostasis.

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“…NGFand BDNF-IRs have been previously found by using ELISA in the MPG ganglia of male rats (Murray et al 2004). Moreover, TrkA-, TrkB-and p75 NTR -IRs have been found by using immunohistochemistry in the majority of neurons of these ganglia (Keast and Kepper, 2001;Murray et al 2004).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, it has been observed that NGF, BDNF and TrkB were expressed in major pelvic ganglion neurons and their expression increased after cyclophosphamide-induced cystitis in rats (Murray et al 2004).…”

confidence: 99%

Effects of castration on the immunoreactivity to NGF, BDNF and their receptors in the pelvic ganglia of the male rat

Squillacioti¹,

Luca²,

Paino³

et al. 2009

Eur J Histochem

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Nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) and are members of the neurotrophin family, a family of neurotrophic factors that also includes neurotrophin (NT) 3 and NT4/5. Neurotrophins have essential roles in the survival, development and differentiation of neurons in the central and peripheral nervous systems. Neurotrophins exert their effects by binding to corresponding receptors which are formed by the tyrosine protein kinases TrkA, TrkB and TrkC, and the low affinity neurotrophic receptor (p75 NTR ). In the present study, using immunohistochemistry and quantitative analysis, we have investigated immunoreactivity to BDNF, NGF, TrkB, p75 NTR and TrkA in the pelvic ganglia of normal and castrated rats. Neurons of the pelvic ganglia expressed both these neurotrophins and their receptors. After castration the immunoreactivity persisted. However, the number of BDNF-and p75 NTR -IR cells statistically significant decreased after castration. These results suggest that castration modulates the expression of neurotrophins and their receptors in pelvic autonomic neurons.

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Cyclophosphamide Induced Cystitis Alters Neurotrophin and Receptor Tyrosine Kinase Expression in Pelvic Ganglia and Bladder

Cited by 87 publications

References 21 publications

Expression of Phosphorylated cAMP Response Element Binding Protein (p-CREB) in Bladder Afferent Pathways in VIP−/− Mice with Cyclophosphamide (CYP)-Induced Cystitis

Expression of Phosphorylated cAMP Response Element Binding Protein (p-CREB) in Bladder Afferent Pathways in VIP−/− Mice with Cyclophosphamide (CYP)-Induced Cystitis

p75 neurotrophin receptor mediates apoptosis in transit-amplifying cells and its overexpression restores cell death in psoriatic keratinocytes

Effects of castration on the immunoreactivity to NGF, BDNF and their receptors in the pelvic ganglia of the male rat

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