Abundance and Significance of Neuroligin-1 and Neurexin II in the Enteric Nervous System of Embryonic Rats

Wang, Dongming; Pan, Jingnian; Song, Guoxin; Gao, Ni; Zheng, Yi; Zhang, Qiangye; Li, Aiwu

doi:10.1155/2017/1209360

Cited by 9 publications

(10 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We have repeated our previous studies [13,14] and confirmed that gene dysplasia of NLs and FN are associated with HSCR. HSCR is divided into three segments:…”

Section: Resultssupporting

confidence: 82%

“…We have found a temporal trend in the abnormal expression of FN, neuroligin-1 (NL1) and neuroligin-2 (NL2) in the diseased intestine of children with HSCR. [13,14] These pieces of evidence led us to hypothesize that the abnormal development of FN, NL1 and NL2 may lead to intestinal lesions but does not explicitly indicate whether there is a real interaction between FN and NLs. Therefore, we further investigated the expression of FN, NL1 and NL2 on different embryonic days and the relationship between them and confirmed the interaction between FN and NLs in this study.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The inverse relationship between fibronectin and neuroligins in the embryonic rat colon

Gao¹,

Hou²,

Zhang³

et al. 2019

Preprint

Self Cite

View full text Add to dashboard Cite

Our previous study identified that the abnormal expression of fibronectin (FN), neuroligin-1 (NL1) and neuroligin-2 (NL2) in the colons of children with Hirschsprung disease (HSCR), but the correlated relationship between the three in the development of the enteric nervous system (ENS) remains unclear. Colons of Wistar rats and PC12 neurons were used to investigate the relationship between FN and the neuroligins (NLs). Colon tissues from thirty healthy embryonic rats, including fifteen at embryonic day 16 (E16), eight at E18, seven at E20, and fifteen newborn rats within 24 hours (Ep0) were analyzed to determine the correlated expression of FN and NLs using Western blot (WB) analysis and real-time fluorescence quantitative PCR (qRT-PCR) methods.Small interfering ribonucleic acid (siRNA) targeting and gene plasmids were used to explore the functional interaction between FN and NLs by using PC12 neuron cells.Furthermore, we used recombinant FN and NL proteins to confirm their interactions.Our studies showed that there were downregulatory effects between FN and the NLs in the embryonic rat colon and different cell lines, indicating that FN and NLs could directly regulate each other, and there is a negative linear correlation between them.The imbalanced interaction between extracellular matrix and synapse-related genes may provide a new perspective for the pathogenesis and treatment of HSCR and neuronal intestinal malformations (NIMs).

show abstract

“…We have repeated our previous studies [13,14] and confirmed that gene dysplasia of NLs and FN are associated with HSCR. HSCR is divided into three segments:…”

Section: Resultssupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

The inverse relationship between fibronectin and neuroligins in the embryonic rat colon

Gao¹,

Hou²,

Zhang³

et al. 2019

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…To clarify potential mechanisms underlying GI dysfunction in neuroligin‐3 linked autism, we characterized expression of neuroligins and their binding partners, the neurexins, in the mouse GI tract. Neuroligins and neurexins are expressed in the rodent [Leembruggen et al, ; Wang et al, ] and human [Wang et al, ; Yang et al, ; Zhang et al, ] GI tract; however, little is known about the functional contribution of neuroligin‐3 expression in the GI tract. Nlgn1 , Nlgn2 , Nlgn3 , Nrxn1 , and Nrxn2 mRNAs are predominantly expressed in myenteric plexus‐enriched preparations of both duodenum and colon (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…These mutations include genes encoding neuroligins, a group of four postsynaptic adhesion molecules (neuroligins‐1 to 4) and their extracellular and intracellular binding partners, neurexins and SHANK3 [Sudhof, ]. Expression of genes encoding several of these proteins is reported in the GI tract [Wang et al, , ; Yang et al, ; Zhang et al, ]; however a systematic analysis of expression in both the small and large intestine and, of particular interest, in neuronal enriched samples is needed.…”

Section: Introductionmentioning

confidence: 99%

Gastrointestinal dysfunction in patients and mice expressing the autism‐associated R451C mutation in neuroligin‐3

et al. 2019

View full text Add to dashboard Cite

Gastrointestinal (GI) problems constitute an important comorbidity in many patients with autism. Multiple mutations in the neuroligin family of synaptic adhesion molecules are implicated in autism, however whether they are expressed and impact GI function via changes in the enteric nervous system is unknown. We report the GI symptoms of two brothers with autism and an R451C mutation in Nlgn3 encoding the synaptic adhesion protein, neuroligin‐3. We confirm the presence of an array of synaptic genes in the murine GI tract and investigate the impact of impaired synaptic protein expression in mice carrying the human neuroligin‐3 R451C missense mutation (NL3 R451C ). Assessing in vivo gut dysfunction, we report faster small intestinal transit in NL3 R451C compared to wild‐type mice. Using an ex vivo colonic motility assay, we show increased sensitivity to GABA A receptor modulation in NL3 R451C mice, a well‐established Central Nervous System (CNS) feature associated with this mutation. We further show increased numbers of small intestine myenteric neurons in NL3 R451C mice. Although we observed altered sensitivity to GABA A receptor modulators in the colon, there was no change in colonic neuronal numbers including the number of GABA‐immunoreactive myenteric neurons. We further identified altered fecal microbial communities in NL3 R451C mice. These results suggest that the R451C mutation affects small intestinal and colonic function and alter neuronal numbers in the small intestine as well as impact fecal microbes. Our findings identify a novel GI phenotype associated with the R451C mutation and highlight NL3 R451C mice as a useful preclinical model of GI dysfunction in autism. Autism Res 2019, 12: 1043–1056 . © 2019 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary People with autism commonly experience gastrointestinal problems, however the cause is unknown. We report gut symptoms in patients with the autism‐associated R451C mutation encoding the neuroligin‐3 protein. We show that many of the genes implicated in autism are expressed in mouse gut. The neuroligin‐3 R451C mutation alters the enteric nervous system, causes gastrointestinal dysfunction, and disrupts gut microbe populations in mice. Gut dysfunction in autism could be due to mutations that affect neuronal communication.

show abstract

“…Immunoblotting analysis was performed as previously described. [7] Blots were incubated overnight at 4ºC with the following primary antibodies:…”

Section: Western Blottingmentioning

confidence: 99%

Dietary Energy Levels from Middle to Late Gestation of Guangdong Small-Ear Spotted Pig: Effects on Body Weight, Muscle Development, and Glucose Metabolism of its Newborn Piglets

Yang

Chen

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Guangdong Small-ear Spotted pigs are Chinese indigenous pig that have the characteristic of desired meat quality and resistance to coarse feeding. However, no study has elucidated the effects of dietary energy levels on body weight, muscle development and glucose metabolism of its newborn piglets. Therefore, a total of 66 pregnant gilts with an average body weight of 80.6±6.6 kg at day 60 of gestation were randomly divided into two groups: control group (CON group; 11.50 MJ/kg digestible energy), and high-energy diet group (HE group; 13.42 MJ/kg digestible energy). Results: The results showed that the maternal HE diet was shown to decrease the birth weight of piglets that from the gilts with total or alive litter size of 12 to 13. Additionally, the HE diet group were shown to impair the glucose tolerance of newborn piglets, as evidenced by the glucose tolerance test and the inhibition of insulin signaling pathway in liver and soleus muscle. Despite no significant change in the muscle weight in the two groups, the maternal HE diet was shown to downregulate the protein level of slow-twitch fiber myosin heavy chain I (MyHC I), and upregulate the protein levels of fast-twitch fiber myosin heavy chain IIb (MyHC IIb) and IIx (MyHC IIx) in soleus muscle of their progeny. Furthermore, the newborn piglets in HE group were showed a decrease in mitochondrial biogenesis in liver and soleus muscle when compared to that in CON group. Conclusions: Maternal high-energy diet from middle to late gestation decreases the birth weight of piglets that from the gilts with total or alive litter size of 12 to 13, induces the formation of glycolytic muscle fibers, and impairs glucose tolerance of their newborn piglets.

show abstract

Abundance and Significance of Neuroligin-1 and Neurexin II in the Enteric Nervous System of Embryonic Rats

Cited by 9 publications

References 27 publications

The inverse relationship between fibronectin and neuroligins in the embryonic rat colon

The inverse relationship between fibronectin and neuroligins in the embryonic rat colon

Gastrointestinal dysfunction in patients and mice expressing the autism‐associated R451C mutation in neuroligin‐3

Dietary Energy Levels from Middle to Late Gestation of Guangdong Small-Ear Spotted Pig: Effects on Body Weight, Muscle Development, and Glucose Metabolism of its Newborn Piglets

Contact Info

Product

Resources

About