# CARTILAGE PROTEINS IN LIGAMENT DEFICIENT KNEES

> **NIH NIH R01** · CLEVELAND CLINIC FOUNDATION · 1989 · $168,907

## Abstract

OSTEOARTHRITIS (OA) is a major cause of disability.  The
majority of clinically demonstrable secondary OA involves some
compromise in joint stability.  Rupture of the ANTERIOR
CRUCIATE LIGAMENT (ACL) is a common SPORTS INJURY and
OA frequently develops as a consequence.  Elucidation of the
molecular and cellular mechanisms in cartilage degeneration
following ACL rupture would provide a rational approach towards
management of this and other types of OA.

Preliminary studies by the P.I. using the canine ACL model of OA
established a marked increase in soluble TYPE VI COLLAGEN in
the OA cartilage compared with controls.  The aims of the
proposed study are to establish the quantities, molecular and
fibrillar forms, tissue distribution, function and the control of
synthesis of TYPE VI collagen in cartilage in the CANINE ACL-
DEFICIENT MODEL.

Quantitation of guanidine soluble Type VI collagen in articular
cartilage of the animal model will be accomplished by ELISA
assays.  Immunoblotting of electrophoretic gels will establish the
molecular forms and immunofluorescence and electron
microscopy the tissue distribution and fibrillar forms of Type VI
collagen.

The function of Type VI collagen in cartilage will be investigated
by measuring its ability to promote attachment of chondrocytes
and to bind proteoglycans, Type II collagen and matrix
glycoproteins from normal and experimental canine OA.

The expression of Type VI collagen will be investigated in tissue
explants and chondrocyte monolayer cultures of canine
chondrocytes.  An in vitro model of limited matrix degradation,
accomplished by enzymatic and interleukin 1 mediated
degradation of normal and experimental OA canine cartilage
explants, will be employed to investigate the capacity of
chondrocytes to synthesize Type VI and Type II collagens and
proteoglycans in damaged matrices.  The control of Type VI
synthesis at the level of translation in normal and OA canine
chondrocytes will be compared by analysis of in vitro translation
products of chondrocyte mRNA.

## Key facts

- **NIH application ID:** 3159698
- **Project number:** 5R01AR039569-02
- **Recipient organization:** CLEVELAND CLINIC FOUNDATION
- **SAM.gov UEI:** TDGUJ1WA4UJ9
- **Principal Investigator:** CAHIR Aidan MCDEVITT
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $168,907
- **Award type:** 5
- **Project period:** 1988-07-01 → 1991-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3159698

## Citation

> US National Institutes of Health, RePORTER application 3159698, CARTILAGE PROTEINS IN LIGAMENT DEFICIENT KNEES (5R01AR039569-02). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3159698. Licensed CC0.

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