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Loss of ADAM29 does not affect viability and fertility in mice but improves wound healing
Diana Campos-Iglesias1,2, Alejandro A Montero1, Francisco Rodríguez3
1Departamento de Bioquímica y Biología Molecular, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, Oviedo, Spain.
Abstract:
ADAM29 (a disintegrin and metalloprotease domain 29) is a member of the membrane-anchored ADAM family of proteins, which is highly expressed in testis and may mediate different physiological and pathological processes. Although the functions of many ADAM family members have been well characterized, the biological relevance of ADAM29 has remained largely unknown. Here, we report the generation of an Adam29-deficient mouse model to delve deeper into the in vivo functions of this ADAM family member. We show that ADAM29 depletion does not affect mice viability, development, or fertility, but somehow impinges on metabolism and energy expenditure. We also report herein that ADAM29 deficiency leads to an accelerated wound healing process, without affecting cell reprogramming in mouse-derived fibroblasts. Collectively, our findings provide new insights into ADAM29 biological functions, highlighting the importance of non-catalytic ADAM proteases.
Insights
ADAM29 (a disintegrin and metalloprotease domain 29) deficiency impacts metabolism and energy expenditure in mice. However, it accelerates wound healing without affecting cell reprogramming.
Area of Science:
- Biochemistry
- Molecular Biology
- Physiology
Background:
- ADAM29 (a disintegrin and metalloprotease domain 29) is a membrane-anchored protein highly expressed in the testis.
- The specific biological functions of ADAM29 remain largely uncharacterized.
- Many other ADAM family members have well-defined roles in various physiological and pathological processes.
Purpose of the Study:
- To investigate the in vivo functions of ADAM29.
- To generate and analyze an Adam29-deficient mouse model.
Main Methods:
- Generation of Adam29-deficient mice.
- Assessment of viability, development, fertility, metabolism, energy expenditure, and wound healing.
- Analysis of cell reprogramming in mouse-derived fibroblasts.
Main Results:
- ADAM29 depletion did not affect mouse viability, development, or fertility.
- ADAM29 deficiency impacted metabolism and energy expenditure.
- Accelerated wound healing was observed in ADAM29-deficient mice.
- Cell reprogramming in mouse-derived fibroblasts was not affected by ADAM29 deficiency.
Conclusions:
- ADAM29 plays a role in regulating metabolism and energy expenditure.
- ADAM29 is involved in the wound healing process.
- These findings highlight the significance of non-catalytic ADAM proteases, specifically ADAM29.
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