Open AccessType XIX collagen: a promising biomarker from the basement membranes
Author(s) -
Ana Cristina Calvo,
Laura Moreno,
Leticia Moreno,
Janne M. Toivonen,
Raquel Manzano,
Nora Molina,
Miriam de la Torre,
Tresa López,
Francisco Javier Miana-Mena,
Marı́a Jesús Muñoz,
Pilar Zaragoza,
P Larrodé,
Alberto García Redondo,
Rosario Osta
Publication year - 2020
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.270299
Subject(s) - basement membrane , amyotrophic lateral sclerosis , collagen, type i, alpha 1 , type i collagen , type iv collagen , chemistry , microbiology and biotechnology , fibril , integrin , extracellular matrix , pathology , cancer research , biology , medicine , laminin , biochemistry , disease , receptor
Among collagen members in the collagen superfamily, type XIX collagen has raised increasing interest in relation to its structural and biological roles. Type XIX collagen is a Fibril-Associated Collagen with Interrupted Triple helices member, one main subclass of collagens in this superfamily. This collagen contains a triple helix composed of three polypeptide segments aligned in parallel and it is associated with the basement membrane zone in different tissues. The molecular structure of type XIX collagen consists of five collagenous domains, COL1 to COL5, interrupted by six non-collagenous domains, NC1 to NC6. The most relevant domain by which this collagen exerts its biological roles is NC1 domain that can be cleavage enzymatically to release matricryptins, exerting anti-tumor and anti-angiogenic effect in murine and human models of cancer. Under physiological conditions, type XIX collagen expression decreases after birth in different tissues although it is necessary to keep its basal levels, mainly in skeletal muscle and hippocampal and telencephalic interneurons in brain. Notwithstanding, in amyotrophic lateral sclerosis, altered transcript expression levels show a novel biological effect of this collagen beyond its structural role in basement membranes and its anti-tumor and anti-angiogenic properties. Type XIX collagen can exert a compensatory effect to ameliorate the disease progression under neurodegenerative conditions specific to amyotrophic lateral sclerosis in transgenic SOD1G93A mice and amyotrophic lateral sclerosis patients. This novel biological role highlights its nature as prognostic biomarker of disease progression in and as promising therapeutic target, paving the way to a more precise prognosis of amyotrophic lateral sclerosis.