Glial-derived neurotrophic factor reduces inflammation and improves delayed colonic transit in rat models of dextran sulfate sodium-induced colitis

Liu, Gong Xiang; Yang, Ying; Yan, Jun; Tao, Zhen; Zou, Yu; Huang, Xiao Li; Gan, Hua

doi:10.1016/j.intimp.2014.01.008

Cited by 25 publications

(10 citation statements)

References 46 publications

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“…Glial‐derived neurotrophic factor was recently shown to have strong anti‐apoptotic effects in colonic epithelial cells in vitro . Glial‐derived neurotrophic factor was reported to partially prevent the loss of enteric neurons, markedly ameliorate experimental colitis, and delay colonic transit by down‐regulating the expression of tumor necrosis factor‐α (TNF‐α) and interleukin‐1β (IL‐1β) expression, decreasing the infiltration of leukocytes, and inhibiting neuronal cell apoptosis …”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐211 causes ganglion cell dysplasia in congenital intestinal atresia via down‐regulation of glial‐derived neurotrophic factor

Xia

Ding

Zhang

et al. 2015

Neurogastroenterology Motil

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐211 causes ganglion cell dysplasia in congenital intestinal atresia via down‐regulation of glial‐derived neurotrophic factor

Xia

Ding

Zhang

et al. 2015

Neurogastroenterology Motil

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“…2). Homeostasis-restoring neuromodulators and hormones as VIP [46,56,57], GLP-2 [58][59][60], pituitary adenylate cyclase-activating polypeptide (PACAP) [61], galanin [62,63], glial-derived neurotrophic factor (GDNF) [64], oxytocin (OT) [65], prostaglandin D2 (PGD2) [66], somatostatin [67,68], dopamine [69] and GABA [70], inhibit the amount of proinflammatory cytokines, stimulate anti-inflammatory cytokines, decrease intestinal permeability and promote neuronal survival. On the other hand, inflammation-maintaining modulators as neurotensin (NT) [71], substance P [72], 5-HT [41,73], neuropeptide Y (NPY) [74,75] and nerve growth factor (NGF) [76] mainly promote pro-inflammatory cytokines and increase intestinal permeability.…”

Section: Linking Gut Inflammation a Predecessor For Crc And The Ensmentioning

confidence: 99%

The role of enteric neurons in the development and progression of colorectal cancer

Rademakers

Vaes

Schonkeren

et al. 2017

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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The enteric nervous system (ENS) is the intrinsic neural network of the gastrointestinal tract, which is essential for regulating gut functions and intestinal homeostasis. The importance of the ENS is underscored by the existence of severe gastrointestinal diseases, such as Hirschsprung's disease and intestinal pseudo-obstruction, which arise when the ENS fails to develop normally or becomes dysregulated. Moreover, it is known that enteric neurons are involved in intestinal inflammation. However, the role of the ENS in colorectal cancer (CRC) carcinogenesis remains poorly understood, even though processes like perineural invasion and neoneurogenesis are important factors in CRC. Here we summarize how enteric neurons are affected during CRC and discuss the influence of enteric neurons, either direct or indirect, on the development and/or progression of CRC. Finally, we illustrate how the ENS could be targeted as a potential anti-cancer therapy, establishing the ENS as an integral part of the tumor microenvironment.

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“…Glial cell line-derived neurotrophic factor (GDNF) is an important neurotrophic factor for ENS, which is related to regulate the proliferation, maturation, and survival of the enteric neurons [10]. GDNF could activate the RET tyrosine kinase receptor, resulting in the stimulation of the phosphoinositide 3-kinase (PI3K) pathway, which is the main signaling pathway for GDNF [11].…”

Section: Introductionmentioning

confidence: 99%

Abdominal Massage Reduces Visceral Hypersensitivity via Regulating GDNF and PI3K/AKT Signal Pathway in a Rat Model of Irritable Bowel Syndrome

Luo

Liu

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Changes in gut motility and visceral hypersensitivity are two major features of irritable bowel syndrome (IBS). Current drug treatments are often poorly efficacious, with many side effects for patients with IBS. Complementary therapies, such as acupuncture or abdominal massage, have received more attention in recent years. In this study, a rat model of IBS with diarrhea (IBS-D) was established by instillation of acetic acid from the colon. The effects of abdominal massage on changes in gut motility, visceral hypersensitivity, and the possible mechanism were investigated. Continuous abdominal massage could decrease the stool consistency score and increase the efflux time of glass beads compared with model groups, while also decreasing mast cell counts in IBS-D rats. The mRNA and protein expressions of neuronal nitric oxide synthase (nNOS), choline acetyl transferase (CHAT), and protein gene product 9.5 (PGP9.5) were significantly upregulated by continuous abdominal massage compared with model groups. Continuous abdominal massage also improved the ultrastructure of enteric glial cells (EGCs) by decreasing the number of mitochondria and increasing the level of the heterochromatin. Meanwhile, continuous abdominal massage could upregulate the expression of glial cell line-derived neurotrophic factor (GDNF) and P-Akt/Akt. Furthermore, it could reduce visceral hypersensitivity and improve the IBS-D symptoms by regulating the phosphoinositide 3-kinase (PI3K)-Akt pathway, which would provide a novel method for the treatment of IBS-D in the clinical setting.

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Glial-derived neurotrophic factor reduces inflammation and improves delayed colonic transit in rat models of dextran sulfate sodium-induced colitis

Cited by 25 publications

References 46 publications

MicroRNA‐211 causes ganglion cell dysplasia in congenital intestinal atresia via down‐regulation of glial‐derived neurotrophic factor

MicroRNA‐211 causes ganglion cell dysplasia in congenital intestinal atresia via down‐regulation of glial‐derived neurotrophic factor

The role of enteric neurons in the development and progression of colorectal cancer

Abdominal Massage Reduces Visceral Hypersensitivity via Regulating GDNF and PI3K/AKT Signal Pathway in a Rat Model of Irritable Bowel Syndrome

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