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Scleral Fibroblasts

Dental Implant Biomaterial and Myopia Research Using Lifeline’s Fibroblasts

Gingival and Scleral Fibroblasts

Fibroblasts are a spindle-shaped cell present in the connective tissue of the body. Their main function is to produce elements of the extracellular matrix, a tissue support network composed of collagen, glycoproteins, and elastin.

Human gingival fibroblasts are located in the periodontal tissue, or gums, in the mouth. They help to maintain homeostasis of the tissue and participate in wound healing when the tissue is injured. Additionally, gingival fibroblasts may contribute to the pathogenesis of periodontal disease through activation of the inflammatory response.

Scleral fibroblasts are located in the sclera, or outer layer, of the eye. In particular, they play a key role in determining the shape of the eye, which may influence the development of near- or far-sightedness.

Check out the Lifeline® catalog for our gingival and scleral fibroblasts, as well as fibroblasts from the following tissues:

Lifeline Normal Human Gingival Fibroblasts in Biomaterial Research

Dental implants are a common dental procedure. Long-term health of dental implants depends on successful osseointegration, the process by which the implant interfaces with the bone to become part of the surrounding bone tissue. Commercially pure titanium (cpTi) is the most commonly used dental implant material, but can it be corroded in the oral environment, causing implant failure. Given this, researchers have evaluated zirconia (ZrO2) as an alternative material for use in dental implants. Successful osseointegration depends on fibroblast attachment and proliferation at the implant site, followed by osteoblast proliferation to generate bone tissue. This process can be subverted by the growth of bacterial biofilms on the implant. Thus, in a study from 2019, Siddiqui and colleagues (opens in new window) compared bacterial and mammalian cell growth and adhesion on cpTi and ZrO2 surfaces. In particular, the authors tested cell growth on cpTi and yttria- or magnesia-stabilized (Y- or Mg-stabilized, respectively) ZrO2 surfaces that were polished, acid-etched, or sandblasted.

They first determined whether the type of surface and surface material would affect growth of Streptococcus mutans, Streptococcus sanguinis, or Streptococcus salivarius. They found that for all three bacteria strains, growth on cpTi or ZrO2 surfaces did not preferentially affect bacterial count; however, during days 1–3 of growth on each surface, S. sanguinis and S. salivarius had higher adherent counts on rougher surfaces (sandblasted and acid-etched, respectively). Next, they evaluated cell proliferation of macrophages, Lifeline® human gingival fibroblasts, and murine pre-osteoblasts on each surface. They demonstrated that after 3 days of growth, acid-etched cpTi supported the highest amount of macrophage and gingival fibroblast proliferation. After 7 days of growth, fibroblast and pre-osteoblast proliferation did not differ across cpTi, Y-ZrO2, and Mg-ZrO2 surfaces.

Overall, the authors concluded that bacterial and mammalian growth on cpTi and ZrO2 surfaces is comparable and both may be used as biomaterials in dental implants.

Lifeline Scleral Fibroblasts in Myopia Research

Myopia, or near-sightedness, can be treated using corrective lenses; however, individuals with highly myopic eyes have an increased risk of developing complications such as cataracts or glaucoma. Therefore, development of therapeutic compounds that block myopia progression in children are of great interest. Atropine, an antimuscarinic agent, has shown promise in myopia prevention studies, but the mechanism by which it works is unknown. Using next-generation sequencing of Lifeline human scleral fibroblasts, Hsiao et al. (opens in new window) set out to determine how atropine treatment affects scleral fibroblast gene expression.

Overall, the authors identified 389 differentially regulated genes (215 upregulated and 174 downregulated) in Lifeline scleral fibroblasts treated with atropine, compared with untreated scleral fibroblasts. Additionally, they found 23 differentially regulated microRNAs (miRNAs), including 15 upregulated and 8 downregulated. Gene ontology and gene set enrichment analyses suggested that the differentially expressed genes were involved in cell differentiation, extracellular matrix-related structural changes, and melatonin signaling. Using mRNA target analyses, the authors next identified 15 candidate genes regulated by the 23 miRNAs whose expression was changed following atropine treatment. Of these, the prolactin receptor (PLRL), potassium voltage-gated channel subfamily J member 5 (KCNJ5), and semaphoring 6A (SEMA6A) were identified as genes of interest that drive scleral fibroblast changes induced by atropine.

Together, the results of this study provide a global picture of the gene expression changes that occur in scleral fibroblasts treated with atropine and may provide future insight into the mechanisms by which atropine exerts a protective effect against myopia.

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