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Investigating the Effect of Inducing a Mammalian-Like Inflammatory Response in Axolotl Regeneration.

Record Type:	Language materials, manuscript : Monograph/item
Title/Author:	Investigating the Effect of Inducing a Mammalian-Like Inflammatory Response in Axolotl Regeneration./
Author:	Garcia Vazquez, Ruben Octavio.
Description:	1 online resource (90 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 84-04, Section: B.
Contained By:	Dissertations Abstracts International84-04B.
Subject:	Genetics. -
Online resource:	click for full text (PQDT)
ISBN:	9798352697382

Investigating the Effect of Inducing a Mammalian-Like Inflammatory Response in Axolotl Regeneration.
Garcia Vazquez, Ruben Octavio.

Investigating the Effect of Inducing a Mammalian-Like Inflammatory Response in Axolotl Regeneration. - 1 online resource (90 pages)

Source: Dissertations Abstracts International, Volume: 84-04, Section: B.

Thesis (Ph.D.)--University of Florida, 2021.

Includes bibliographical references

Wound healing in adult mammals is characterized by inflammation followed by extensive collagen deposition that leads to fibrotic scarring. Macrophages, key components of the immune system as both effector and paracrine cells, play an essential role in regulating mammalian wound healing and scarification. They are also imperative in the process of regeneration of both mammals and axolotls. Axolotl's regenerative ability allows them to heal wounds without scarring and regenerate limbs. Previous research depicts mammals exhibiting a high initial inflammatory phase during regeneration where macrophages are polarized towards a pro-inflammatory phenotype, leading to incomplete regeneration and scarification. In contrast, preliminary studies show that axolotl macrophages do not respond to injury by polarizing into pro-inflammatory phenotypes. Comparative studies between axolotl regeneration and mammalian wound healing stipulate that axolotl have a significantly lower inflammation onset at the wounding time along with lower collagen depositions in comparison to mammals. Low to no inflammatory response during wound healing and no fibrotic scarring leads to the hypothesis that an inflammatory macrophage response is responsible for high collagen depositions that in return causes scarring. Importantly, they show that inducing an inflammatory response blocks regeneration and leads to fibrotic, mammalian-like scars. This study tests axolotl macrophages' ability to polarize into either M1 or M2 and their capability to have an inflammatory phenotype. The overall goal is to use comparative biology to define the pathways that promote scar-free healing in axolotls versus scarification in mice/humans.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798352697382Subjects--Topical Terms:

578972
Genetics.
Subjects--Index Terms:

AxolotlIndex Terms--Genre/Form:

554714
Electronic books.

Investigating the Effect of Inducing a Mammalian-Like Inflammatory Response in Axolotl Regeneration.
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520 $a Wound healing in adult mammals is characterized by inflammation followed by extensive collagen deposition that leads to fibrotic scarring. Macrophages, key components of the immune system as both effector and paracrine cells, play an essential role in regulating mammalian wound healing and scarification. They are also imperative in the process of regeneration of both mammals and axolotls. Axolotl's regenerative ability allows them to heal wounds without scarring and regenerate limbs. Previous research depicts mammals exhibiting a high initial inflammatory phase during regeneration where macrophages are polarized towards a pro-inflammatory phenotype, leading to incomplete regeneration and scarification. In contrast, preliminary studies show that axolotl macrophages do not respond to injury by polarizing into pro-inflammatory phenotypes. Comparative studies between axolotl regeneration and mammalian wound healing stipulate that axolotl have a significantly lower inflammation onset at the wounding time along with lower collagen depositions in comparison to mammals. Low to no inflammatory response during wound healing and no fibrotic scarring leads to the hypothesis that an inflammatory macrophage response is responsible for high collagen depositions that in return causes scarring. Importantly, they show that inducing an inflammatory response blocks regeneration and leads to fibrotic, mammalian-like scars. This study tests axolotl macrophages' ability to polarize into either M1 or M2 and their capability to have an inflammatory phenotype. The overall goal is to use comparative biology to define the pathways that promote scar-free healing in axolotls versus scarification in mice/humans.
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