Collagenolytic activity in regenerating forelimbs of the adult newt (Triturus viridescens)

https://doi.org/10.1016/0012-1606(68)90006-7Get rights and content

Summary

A collagenolytic enzyme capable of degrading reconstituted collagen fibrils at neutral pH and physiological temperature, not demonstrable in the intact forelimb of the adult newt (Triturus viridescens) appears in cultures of healing and regenerating tissues of the amputation stump. Tissues proximal to the regenerating region are inactive. The amount of enzyme produced, measured by visible breakdown of thermally reconstituted mammalian collagen gels, and confirmed by release of radioactivty from14C-glycine-labeled collagen gels, rises to a peak at 15 days and remains at a high level during the phases of dedifferentiation of the stump and blastema formation, but gradually falls after 20 days as early digital differentiation occurs. Living cells are required for collagenase production since freezing and thawing inactivates the explants.

References (21)

There are more references available in the full text version of this article.

Cited by (90)

  • Animal models of skin regeneration

    2014, Reproductive Biology
    Citation Excerpt :

    The high and sustained levels of HA in nude skin could account for the significant increase in elasticity of post-injured nude skin tissue [21]. The pivotal role of matrix metalloproteinanses (MMPs) in regeneration has been contemplated since Grillo and co-workers demonstrated a collagenolytic activity in the regenerating limbs of newts that was absent from non-regenerating limbs [39]. Then Vinarsky and co-workers showed that MMPs are required for normal limb regeneration [40] and blockage of MMPs activity caused failure of limb regeneration in newts and formation of scar-like structures at the end of the limb stump.

  • Histochemical, Biochemical and Cell Biological aspects of tail regeneration in lizard, an amniote model for studies on tissue regeneration

    2014, Progress in Histochemistry and Cytochemistry
    Citation Excerpt :

    An increase of a likely GAG degrading enzyme, beta-glucuronidase was reported in the wound-healing phase but the activity and localization of the enzyme also in later stages, especially in the basal layer of the epidermis, was correlated to the protein biosynthesis in proliferating cells more than with degradation of extracellular matrix (Shah and Hiradhar, 1976). Until recently is was not known whether specific collagenases that degrade and maintain the collagen level low like in amphibian blastema (Grillo et al., 1968), are also activated in the lizard blastema. However the increase of acid phosphatase during tail regeneration (Shah and Chakko, 1966; Varughese et al., 1980; Alibardi, 1998) indicated that degrading lysosomal enzymes are activated in the wound healing, blastema and during early growth of the regenerating lizard tail.

  • Matrix metalloproteinases (MMPs) are required for wound closure and healing during larval leg regeneration in the flour beetle, Tribolium castaneum

    2012, Insect Biochemistry and Molecular Biology
    Citation Excerpt :

    MMPs contribute to healing by acting as proteinases that degrade the extracellular matrix and regulate the activity of signaling molecules and growth factors (Nagase and Woessner, 1999). In urodeles, MMP expression and activity increases in the wound epithelial cells following limb amputation and is necessary for limb regeneration (Campbell and Crews, 2008; Grillo et al., 1968; Miyazaki et al., 1996; Park and Kim, 1999; Vinarsky et al., 2005; Yang and Bryant, 1994; Yang et al., 1999). The second step of limb regeneration in vertebrates involves the formation of a blastema at the wound site.

  • Mechanisms of Blastema Formation in Regenerating Amphibian Limbs

    2010, Principles of Regenerative Medicine, Second Edition
View all citing articles on Scopus

This investigation was supported by Public Health Service Research Grant CA-03638 from the National Cancer Institute, Grant AM3564 from the United States Public Health Service and Grant AM5142 from the National Institute of Arthritis and Metabolic Diseases.

This is publication No. 451 of the Robert W. Lovett Memorial Group for the Study of Disease Causing Deformities, Massachusetts General Hospital, Boston, Massachusetts.

This work in preliminary form has been reported earlier in a symposium (Grillo, 1964).

View full text