| First Author | Qiu D | Year | 2021 |
| Journal | Metabolism | Volume | 114 |
| Pages | 154412 | PubMed ID | 33164859 |
| Mgi Jnum | J:341856 | Mgi Id | MGI:6750971 |
| Doi | 10.1016/j.metabol.2020.154412 | Citation | Qiu D, et al. (2021) ICAM-1 deletion delays the repair process in aging diabetic mice. Metabolism 114:154412 |
| abstractText | BACKGROUND: The delayed repair process in the aging diabetic population is becoming an alarming public health concern. ICAM-1 plays an important role in orchestrating the repair process by mediating neutrophil recruitment and phagocytosis. However, little is known about the role of ICAM-1 in aging diabetic repair. METHODS: By causing injury in aging diabetic mice with ICAM-1 deletion (AD-ICAM-1(-/-)), we found that AD-ICAM-1(-/-) mice exhibited a delayed repair process with incomplete re-epithelialization and reduced angiogenesis. Additionally, high-throughput Illumina sequencing was performed to evaluate the microbiota of such mice. RESULTS: The results indicate that the microbiota of the AD-ICAM-1(-/-) injury site differed taxonomically at both the phylum and genus levels. Neutrophil recruitment and phagocytic function were also reduced in the AD-ICAM-1(-/-) group. Notably, major inflammatory biomarker expression was also detected in AD-ICAM-1(-/-) injured tissue. CONCLUSIONS: Overall, this study demonstrated that AD-ICAM-1(-/-) mice exhibit delayed repair. In addition, neutrophil recruitment and phagocytic activity were impaired in the AD-ICAM-1(-/-) group, which may have allowed microbes to colonize the injury site. |
