Defective development and microcirculation of intestine in Npr2 mutant mice
| Autor: | Atsuki Hanagata, Yasuhiro Fujiwara, Chizuru Sogawa-Fujiwara, Masatoshi Hori, Tetsuo Kunieda, Yukisato Ishida, Hirotaka Tomiyasu, Hirofumi Nakatomi |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male Pathology medicine.medical_specialty lcsh:Medicine White adipose tissue Pathogenesis Article Microcirculation 03 medical and health sciences symbols.namesake Mice 0302 clinical medicine Developmental biology medicine Lymphatic vessel Animals lcsh:Science Cyclic GMP Mice Knockout Multidisciplinary business.industry lcsh:R Gastroenterology Lipid metabolism NPR2 Pathophysiology Interstitial cell of Cajal Gastrointestinal Tract Intestines Mice Inbred C57BL Intestinal Diseases 030104 developmental biology medicine.anatomical_structure symbols Female lcsh:Q business Receptors Atrial Natriuretic Factor 030217 neurology & neurosurgery Blood vessel Signal Transduction |
| Zdroj: | Scientific Reports Scientific Reports, Vol 10, Iss 1, Pp 1-14 (2020) |
| ISSN: | 2045-2322 |
| Popis: | Intractable gastrointestinal (GI) diseases often develop during infancy. Our group previously reported that natriuretic peptide receptor B (NPR-B)-deficient Npr2slw/slw mice exhibit severe intestinal dysfunction, such as stenosis and distention, which resembles the dysfunction observed in Hirschsprung’s disease-allied disorders. However, the root cause of intestinal dysfunction and the detailed of pathophysiological condition in the intestine are not yet clear. Here, we report that the intestine of preweaning Npr2slw/slw 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 Npr2slw/slw mice. Moreover, intramuscular interstitial cells of Cajal (ICC-IM) were clearly reduced. In contrast, villi and ICC-IM were developed normally in surviving adult Npr2slw/slw mice. However, adult Npr2slw/slw mice exhibited partially hypoplastic blood vessels and an atrophied enteric nervous. Furthermore, adult Npr2slw/slw mice showed markedly reduced white adipose tissue. These findings suggest that the cause of GI dysfunction in preweaning Npr2slw/slw 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|