Quantitative RT-PCR analysis of total RNA from rat ovaries and in situ hybridisation studies revealed presence of LOX, BMP-1 and PCPE mRNA in both GC and TC of rat ovary. In immature follicles, LOX mRNA principally located to GC where its abundance declined during gonadotrophin induced follicular development. Conversely, BMP-1 and PCPE mRNA were present at similar levels in GC and TC, no developmental regulation was determined in isolated cells but visualisation saw these genes associated with the theca layer declining as maturation occurred. LOX and BMP-1 protein were located in both GC and TC layers. These results suggest a two-cell mechanism of ECM formation involving GC LOX and TC BMP-1. GC and TC isolated from rat ovarian follicles were cultured with development-associated regulatory cues FSH (GC), LH (TC) and TGF-β for immature follicles; LH, TGF-β and IL-1α for preovulatory follicles in presence and absence of anti-inflammatory steroids (progesterone or corticosterone), to determine how these factors affect collagen pathway gene expression in vitro. Results established that components of ECM remodelling were regulated by the changing profile of ovarian regulators. In the immature follicle FSH in the GC, LH in the TC and TGF-β in both cell types causes an overall increase in up-regulation of collagen pathway biology to allow for follicle growth. Towards ovulation LH, progesterone, IL-1 and a lack of TGF-β caused a cessation of active remodelling. Then post-ovulation remodelling was again active due to the positive influences by TFG-β and corticosterone. The conclusion of this thesis is that there are changes in intrafollicular ECM modelling driven by endocrine, paracrine and intracrine signals. Collagen pathway components are key to this process and present targets for future studies of tissue injury and repair in ovary and elsewhere in the body.