The Department of Genetic Medicine at Weill Cornell leads a dynamic and innovative translational research program, advancing diverse fields such as Genetic Therapy and Personalized Medicine.
Our translational research program aims to leverage our expertise in genetic therapies and personalized medicine to develop clinical solutions that target the molecular causes of human diseases.
The Department of Genetic Medicine advances treatments and diagnostics through diverse clinical trials, including drug testing and research to better understand diseases.
The Department of Genetic Medicine at Weill Cornell leads a dynamic and innovative translational research program, advancing diverse fields such as Genetic Therapy and Personalized Medicine.
Our translational research program aims to leverage our expertise in genetic therapies and personalized medicine to develop clinical solutions that target the molecular causes of human diseases.
The Department of Genetic Medicine advances treatments and diagnostics through diverse clinical trials, including drug testing and research to better understand diseases.
Chronic inflammatory processes frequently lead to the abnormal replacement of normal tissue elements by increased numbers of fibroblasts and fibrous connective tissue, i.e., fibrosis. Since the growth of fibroblasts requires that these cells be attached to an extracellular support, the current study was designed to determine if the interaction between the fibroblast attachment factor fibronectin and the C1q component of complement could support fibroblast attachment and growth and thus could form a basis for the attachment of fibroblasts in abnormal tissue locations in those inflammatory states where C1q is bound. Fibronectin purified from human plasma supported attachment of both Chinese hamster ovary cells and of normal fetal lung fibroblasts (HFL-1) to C1q coated substrates. The attachment activity was approximately twice that of attachment to collagen, and was specific, as no attachment occurred to albumin coated substrates. Cells attached to C1q substrates demonstrated characteristic 'spreading' similar to those on collagen. Moreover, the C1q substrate resembled collagen in its ability to support fibroblast growth. Further, the ability of the interaction between C1q and fibronectin to mediate attachment of fibroblasts to immune complexes was demonstrated by the formation of fibroblast-red blood cell-immune complex rosettes, a process that was dependent on both fibronectin and C1q. Thus, the interaction between fibronectin and C1q could serve as the basis for fibroblast attachment and growth in abnormal tissue sites where immune complexes are formed and could be a contributing factor to the development of fibrosis.