Brain‐derived neurotrophic factor accelerates gut motility in slow‐transit constipation

Chen, F.; Yu, Yanbo; Wang, P.; Dong, Yanyan; Wang, T.; Zuo, Xiuli; Li, Y.

doi:10.1111/apha.12374

Cited by 42 publications

(43 citation statements)

References 38 publications

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“…BDNF enhanced peristalsis in the rat colon, and BDNF +/‐ mice had delayed gastrointestinal transit, slow velocity of fecal pellet propulsion, and decreased stool frequency . BDNF levels were significantly reduced in colonic biopsies from patients with slow transit constipation . All the evidence mentioned above indicates that BDNF has prokinetic effects on gut motility.…”

Section: Neurotrophic Factors and Gut Motilitymentioning

confidence: 94%

“…The neural blocker tetrodotoxin failed to block BDNF‐induced enhancement of cholinergic contraction in isolated longitudinal muscle‐myenteric plexus strips from the rabbit jejunum . However, tetrodotoxin attenuated BDNF‐induced augmentation of contraction in the longitudinal muscle‐myenteric plexus strips from the mouse colon . Interestingly, exogenous BDNF had no effect on the basal tone or spontaneous phasic contraction in isolated smooth muscle strips from the rabbit jejunum and mouse ileum and colon, but increased spontaneous phasic contraction in the isolated longitudinal muscle‐myenteric plexus strips from the mouse colon .…”

Section: Neurotrophic Factors and Gut Motilitymentioning

confidence: 94%

“…In fasting rats, exogenous BDNF increased myoelectric activity in the gastrointestinal tract . BDNF enhanced peristalsis in the rat colon, and BDNF +/‐ mice had delayed gastrointestinal transit, slow velocity of fecal pellet propulsion, and decreased stool frequency . BDNF levels were significantly reduced in colonic biopsies from patients with slow transit constipation .…”

Section: Neurotrophic Factors and Gut Motilitymentioning

confidence: 99%

“…However, tetrodotoxin attenuated BDNF‐induced augmentation of contraction in the longitudinal muscle‐myenteric plexus strips from the mouse colon . Interestingly, exogenous BDNF had no effect on the basal tone or spontaneous phasic contraction in isolated smooth muscle strips from the rabbit jejunum and mouse ileum and colon, but increased spontaneous phasic contraction in the isolated longitudinal muscle‐myenteric plexus strips from the mouse colon . Thus, it is unclear whether BDNF can initiate smooth muscle contraction by itself or it merely augments contraction elicited by other excitatory neurotransmitters.…”

Section: Neurotrophic Factors and Gut Motilitymentioning

confidence: 99%

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Neurotrophic factors in enteric physiology and pathophysiology

Liu

2018

Neurogastroenterology Motil

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Neurotrophic factors are traditionally recognized for their roles in differentiation, growth, and survival of specific neurons in the central and peripheral nervous system. Some neurotrophic factors are essential for the development and migration of the enteric nervous system along the fetal and post-natal gut. Over the last two decades, several non-developmental functions of neurotrophic factors have been characterized. In the adult gastrointestinal tract, neurotrophic factors regulate gut sensation, motility, epithelial barrier function, and protect enteric neurons and glial cells from damaging insults in the microenvironment of the gut. In this issue of Neurogastroenterology and Motility, Fu et al. demonstrate that brain-derived neurotrophic factor plays a role in the pathogenesis of distention-induced abdominal pain in bowel obstruction. In light of this interesting finding, this mini-review highlights some of the recent advances in understanding of the physiological and pathophysiological roles of neurotrophic factors in the adult gut.

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Section: Neurotrophic Factors and Gut Motilitymentioning

confidence: 94%

Section: Neurotrophic Factors and Gut Motilitymentioning

confidence: 94%

Section: Neurotrophic Factors and Gut Motilitymentioning

confidence: 99%

Section: Neurotrophic Factors and Gut Motilitymentioning

confidence: 99%

See 2 more Smart Citations

Neurotrophic factors in enteric physiology and pathophysiology

Liu

2018

Neurogastroenterology Motil

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“…In the gut, BDNF has also been shown to have important roles in augmenting the peristaltic reflex by enhancing serotonin (5‐HT) and CGRP (calcitonin gene‐related peptide) release from enteroendocrine cells and enteric sensory neurons, respectively, in augmenting calcium responses in enteric neurons elicited by neurotransmitters thereby enhancing synaptic communication within the enteric nervous system, increasing colonic myoelectrical activity, and enhancing the response of SMCs to contractile agonists . In humans, BDNF increases gut motility, accelerates colonic transit, and increases stool frequency without affecting stool consistency . Brain‐derived neurotrophic factor has a key role in the interrelationship between the central nervous system and the gut.…”

Section: Introductionmentioning

confidence: 99%

Stimulation of synthesis and release of brain‐derived neurotropic factor from intestinal smooth muscle cells by substance P and pituitary adenylate cyclase‐activating peptide

Qudah

Alkahtani

Akbarali

et al. 2015

Neurogastroenterology Motil

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Background Brain-derived neurotrophic factor (BDNF) is a neurotrophin present in the intestine where it participates in survival and growth of enteric neurons, augmentation of enteric circuits, and stimulation of intestinal peristalsis and propulsion. Previous studies largely focused on the role of neural and mucosal BDNF. The expression and release of BDNF from intestinal smooth muscle and the interaction with enteric neuropeptides has not been studied in gut. Methods The expression and secretion of BDNF from smooth muscle cultured from rabbit longitudinal intestinal muscle in response to substance P and pituitary adenylate cyclase activating peptide (PACAP) was measured by western blot and ELISA. BDNF mRNA was measured by rt-PCR. Key Results The expression of BNDF protein and mRNA was greater in smooth muscle cells from the longitudinal muscle than from circular muscle layer. PACAP and substance P increased the expression of BDNF protein and mRNA in cultured longitudinal smooth muscle cells. PACAP and substance P also stimulated the secretion of BDNF from cultured longitudinal smooth muscle cells. Chelation of intracellular calcium with BAPTA prevented substance P-induced increase in BDNF mRNA and protein expression as well as substance P-induced secretion of BDNF. Conclusions & Inferences Neuropeptides known to be present in enteric neurons innervating the longitudinal layer increase the expression of BDNF mRNA and protein in smooth muscle cells and stimulate the release of BDNF. Considering the ability of BDNF to enhance smooth muscle contraction, this autocrine loop may partially explain the characteristic hypercontractility of longitudinal muscle in inflammatory bowel disease.

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Advanced statistics identification of participant and treatment predictors associated with severe adverse effects induced by fluoropyrimidine-based chemotherapy

Korver

Bowen

Gibson

et al. 2023

Cancer Chemother Pharmacol

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Purpose Adverse effects following fluoropyrimidine-based chemotherapy regimens are common. However, there are no current accepted diagnostic markers for prediction prior to treatment, and the underlying mechanisms remain unclear. This study aimed to determine genetic and non-genetic predictors of adverse effects. Methods Genomic DNA was analyzed for 25 single nucleotide polymorphisms (SNPs). Demographics, comorbidities, cancer and fluoropyrimidine-based chemotherapy regimen types, and adverse effect data were obtained from clinical records for 155 Australian White participants. Associations were determined by bivariate analysis, logistic regression modeling and Bayesian network analysis. Results Twelve different adverse effects were observed in the participants, the most common severe adverse effect was diarrhea (12.9%). Bivariate analysis revealed associations between all adverse effects except neutropenia, between genetic and non-genetic predictors, and between 8 genetic and 12 non-genetic predictors with more than 1 adverse effect. Logistic regression modeling of adverse effects revealed a greater/sole role for six genetic predictors in overall gastrointestinal toxicity, nausea and/or vomiting, constipation, and neutropenia, and for nine non-genetic predictors in diarrhea, mucositis, neuropathy, generalized pain, hand–foot syndrome, skin toxicity, cardiotoxicity and fatigue. The Bayesian network analysis revealed less directly associated predictors (one genetic and six non-genetic) with adverse effects and confirmed associations between six adverse effects, eight genetic predictors and nine non-genetic predictors. Conclusion This study is the first to link both genetic and non-genetic predictors with adverse effects following fluoropyrimidine-based chemotherapy. Collectively, we report a wealth of information that warrants further investigation to elucidate the clinical significance, especially associations with genetic predictors and adverse effects.

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Brain‐derived neurotrophic factor accelerates gut motility in slow‐transit constipation

Abstract: BDNF plays an important regulatory role in gut motility in STC. It was mediated by altering the intestinal innervation structure, as well as smooth muscle secondary degeneration through a mechanism involving TrkB-PLC/IP3 pathway activation.

Cited by 42 publications

References 38 publications

Neurotrophic factors in enteric physiology and pathophysiology

Neurotrophic factors in enteric physiology and pathophysiology

Stimulation of synthesis and release of brain‐derived neurotropic factor from intestinal smooth muscle cells by substance P and pituitary adenylate cyclase‐activating peptide

Advanced statistics identification of participant and treatment predictors associated with severe adverse effects induced by fluoropyrimidine-based chemotherapy

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