Fibroblasts, a heterogenous cell population, are involved in many important functions, such as wound healing. In the central nervous system, fibroblasts are mainly located in the meninges and perivascular space. Mounting evidence suggests that fibroblasts are activated and contribute to fibrotic scar formation, which plays different roles in various neurological disorders. However, the functions of fibroblasts in intracerebral hemorrhage (ICH) remains unknown. This dissertation aims to examine the roles of fibroblasts and fibroblast-derived molecules in ICH. In manuscript #1, we examined the functions of fibroblasts in ICH using fibroblast-ablated mutant mice by targeting fibroblast specific marker Col1α1. These mutants failed to show obvious defects under homeostatic conditions. However, these mutants showed exacerbated blood-brain barrier (BBB) damage, enlarged injury volume and worse neurological function, highlighting a beneficial role of Col1α1+ fibroblasts in ICH. Echoed with these findings, fibroblasts significantly decreased endothelial permeability in an in vitro ICH model. Next, we demonstrated that fibroblasts promoted BBB integrity in ICH via up-regulating tight junction proteins without affecting transcytosis-associated proteins, indicating a paracellular rather than transcellular mechanism. Subsequent mechanistic study revealed that the BBB-protecting effect of fibroblasts is partially mediated by TIMP2. Together, these results suggest that Col1α1+ fibroblasts repair BBB damage in ICH via the paracellular pathway in a TIMP2-dependent manner. Fibroblasts up-regulate the expression of extracellular matrix (ECM) proteins upon injury. Previous studies from our laboratory and others find that laminin, a major ECM protein, actively regulates BBB integrity and stroke outcome. In manuscript #2, the functions of fibroblast-derived ECM protein—laminin was examined using in vivo model. Laminin deficiency in Col1a1+ fibroblast-like cells leads to worse ICH outcome, including enhanced BBB permeability, elevated inflammatory cell infiltration, larger hematoma size, worse neurological dysfunction, increased neuronal cell death, decreased TJ protein level and decreased pericyte coverage. In addition, substantially decreased Col1 deposition was observed at the peri-hematoma region in these mutants at day 7 after injury. Findings from these studies provide valuable insights on the roles of fibroblasts in ICH and new fibroblast-derived molecules identified in this study may be targeted in the treatment of ICH.