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Our group previously reported that natriuretic peptide receptor B (NPR-B)-deficient <jats:italic>Npr2<\/jats:italic><jats:sup><jats:italic>slw\/slw<\/jats:italic><\/jats:sup> mice exhibit severe intestinal dysfunction, such as stenosis and distention, which resembles the dysfunction observed in Hirschsprung\u2019s disease-allied disorders.\u00a0However,\u00a0the root cause of intestinal dysfunction and\u00a0the detailed of pathophysiological condition in the intestine are not yet clear.\u00a0Here, we report that the intestine of preweaning <jats:italic>Npr2<\/jats:italic><jats:sup><jats:italic>slw\/slw\u00a0<\/jats:italic><\/jats:sup>mice showed bloodless blood vessels, and nodes were found in the lymphatic vessel. Additionally, the lacteals, smooth muscle, blood vessel, and nerves were barely observed in the villi of preweaning <jats:italic>Npr2<\/jats:italic><jats:sup><jats:italic>slw\/slw<\/jats:italic><\/jats:sup> mice. Moreover, intramuscular interstitial cells of Cajal (ICC-IM) were clearly reduced. In contrast, villi and ICC-IM were developed normally in surviving adult <jats:italic>Npr2<\/jats:italic><jats:sup><jats:italic>slw\/slw<\/jats:italic><\/jats:sup> mice. However, adult\u00a0<jats:italic>Npr2<\/jats:italic><jats:sup><jats:italic>slw\/slw<\/jats:italic><\/jats:sup> mice exhibited partially hypoplastic blood vessels and an atrophied enteric nervous. Furthermore, adult <jats:italic>Npr2<\/jats:italic><jats:sup><jats:italic>slw\/slw<\/jats:italic><\/jats:sup> mice showed markedly reduced white adipose tissue. These findings suggest that the cause of GI dysfunction in preweaning <jats:italic>Npr2<\/jats:italic><jats:sup><jats:italic>slw\/slw<\/jats:italic><\/jats:sup> mice is attributed to defective intestinal development with microcirculation disorder. Thus, it is suggested that NPR-B signaling is involved in intestinal development and control of microcirculation and fat metabolism. This report provides new insights into intractable GI diseases, obesity, and NPR-B signaling.<\/jats:p>","DOI":"10.1038\/s41598-020-71812-2","type":"journal-article","created":{"date-parts":[[2020,9,10]],"date-time":"2020-09-10T06:23:32Z","timestamp":1599719012000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Defective development and microcirculation of intestine in Npr2 mutant mice"],"prefix":"10.1038","volume":"10","author":[{"given":"Chizuru","family":"Sogawa-Fujiwara","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Atsuki","family":"Hanagata","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasuhiro","family":"Fujiwara","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yukisato","family":"Ishida","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hirotaka","family":"Tomiyasu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tetsuo","family":"Kunieda","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hirofumi","family":"Nakatomi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masatoshi","family":"Hori","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2020,9,8]]},"reference":[{"key":"71812_CR1","doi-asserted-by":"publisher","first-page":"94","DOI":"10.1016\/j.semcdb.2017.01.006","volume":"66","author":"N Nagy","year":"2017","unstructured":"Nagy, N. & Goldstein, A. 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