Introduction to Fibroblast Growth Factor Clinical Study
Fibroblast Growth Factors, or FGFs, are a family of growth factors involved in angiogenesis, wound healing, and embryonic development. They are heparin-binding proteins, and interactions with cell surface-associated heparan sulfate proteoglycans are necessary for FGF signal transduction.
FGFs are small polypeptide growth factors that share common structural characteristics and bind heparin. They contain signal peptides for secretion and can bind to heparin-like glycosaminoglycans (HLGAGs) in the extracellular matrix (ECM).
They can act directly on target cells or be released through the digestion of the ECM or the activity of a secreted FGF-binding protein.
FGFs bind receptor tyrosine kinases in the context of HLGAGs, inducing receptor activation and signal transduction cascades. FGFs are involved in embryonic development and wound healing, and some are potent angiogenic factors.
FGF signaling may also contribute to tumor growth and angiogenesis, and autocrine FGF signaling could be crucial in the progression of steroid hormone-dependent cancers to hormone-independent states.
Some FGFs are potent angiogenic factors, and most play important roles in embryonic development and wound healing. FGF signaling also appears to play a role in tumor growth and angiogenesis, and autocrine FGF signaling may be particularly important in the progression of steroid hormone-dependent cancers to a hormone-independent state. [PDR]
Etymology
- Fibroblasts (FB) are the basic building block of fibrous tissue that includes the brain, nervous system, eye, blood vessels, heart, stomach, skin, liver, kidney, muscle & bone.
- The main function of fibroblasts is to maintain the structural integrity of connective tissues.
- Growth Factors (GF) are the most common cells of connective tissues in the body.
- The suffix “Blast” is used in cellular biology to denote a stem cell or a cell in an “Activated state of metabolism.”
Key Points of FGF
- FGF is responsible for signaling cell restoration, repair, & rejuvenation.
- FGFs are key players in the proliferation and differentiation of cells and tissues.
- FGF is responsible for signaling cell restoration, repair, & rejuvenation.
FGFs are key players in the proliferation of cell tissues.
A detailed day‐by‐day study was performed in 1988 (A4, A11). Discovered only in the seventies and also a peptide, this FGF is critical in the development of embryos, including humans. However, it is not found to be circulating in human adult bodies.
Nerve and tissue growth factors
Nerve growth factor (NGF) is a small protein important for the growth, maintenance, and survival of certain neurons (nerve cells). It also functions as a signaling molecule. NGF induces cellular proliferation, differentiation, and survival. [1]
Connective tissue growth factor (CTGF) is a cysteine-rich protein. CTGF is involved in cell adhesion, migration, proliferation, angiogenesis, skeletal development, and tissue wound repair, including fibrotic disease and several forms of cancers.
The fibroblast is the most common type of cell found in connective tissue. Fibroblasts secrete collagen proteins that are used to maintain a structural framework for many tissues. They play a critical role in wound healing. Fibroblasts are the most common cells of connective tissue in animals.
Active metabolism
Fibroblasts and fibrocytes are two states of the same cells, the former being the activated state, the latter the less active state, concerned with maintenance and tissue metabolism.
Currently, there is a tendency to call both forms fibroblasts. The suffix “blast” is used in cellular biology to denote a stem cell or a cell in an activated state of metabolism.
In recent years, the popularity of Fibroblast Growth Factor (FGF) in the mainstream has brought together this time Pharmaceutical company who wants to incorporate the ingredient into their drugs or medicine.
Independent Research Groups
From 2010 to the present, several medical conventions on FGF were conducted and participated by large Pharmaceutical corporations through the Gordon Institute, such as Aveo, Genentech, Merck Serono, Sanofi Aventis, Amgen, and the National Institutes of Health (NIH).
General References:
Journal Frontier: FGF2 in biological process.
NCBI
PNAS: Neurogenesis in brain injury.
NCBI: Induced cardioprotection against myocardial infarction.
SBRC: FGF-2 in Acute and Chronic Cardiac Response to Injury
(1) Roberts, Pamela R, et al. Nutrition Vol. 14, No. 3, 1998
(2) Kuljis, Rodrigo O. Jour. of Neuropathology & Exp. Neur., 1994.
(3) Jiangyong Min, et al. Jour. of Neuroscience Res., 86:2984‐2991 (2008)
(4) Z.Y. Zhou, et al. Neuroscience, Vol. 90, No. 4, 1493‐1499, 1999
(5) Arvanitakis, Constantine. Am. Jour. of Physiology, Vol. 231, No. 1, July 1976.
(6) Kristoffer, ester S., ETC Research & Development, Oslo, Norway.
(A1) Joseph‐Silverstein, Jacquelyn, et al (June 1989) Basic Fibroblast Growth Factor in the Chick Embryo: Immunolocalization to Striated Muscle Cells and Their Precursors. The Journal of Cell Biology, 108: 2459‐2466.
(A2) Hatten, M. E., et al (1988) In Vitro Neurite Extension by Granule Neurons is Dependent upon Astroglial‐Derived Fibroblast Growth Factor. Developmental Biology, 125:280‐289.
(A4) Seed, Jennifer, et al (1988) Fibroblast Growth Factor Levels in the Whole Embryo and Limb Bud during Chick Development. Developmental Biology, 128:50‐57.
(A11) Seed, Jennifer, et al (1988) Fibroblast Growth Factor Levels in the Whole Embryo and Limb Bud during Chick Development. Developmental Biology, 128:50‐57.
(A14) La Spada, Albert R (December 2005) Huntington’s disease and Neurogenesis: FGF‐2 to the Rescue? Vol. 102.
(A24) Hagg, Theo (2005) Molecular Regulation of Adult CNS Neurogenesis: an Integrated View.
(A25) Bjugstad, K. B., et al (2001) IGF‐1 and bFGF Reduce Glutaric Acid and 3‐ Hydroxyglutaric Acid Toxicity in Striatal Cultures.
(A26) Altman, J. (1962) Science 132:1127‐1128.
(A27) Arlotta, P., et al (2003) Exp. Gerontol, 38:173‐182.
