Hans Peter BächingerKazunori MizunoJanice A. VrankaSergei P. Boudko, in Comprehensive Natural Products II, 2010, Type III collagen belongs to the fibrillar collagen group. Type IV EDS results from defects in the structure or synthesis of type III collagen. Increased amounts of type III collagen are found in many fibrotic conditions such as liver and kidney fibrosis, and systemic sclerosis. Its metabolism can be monitored by assaying the amino-terminal propeptide of type III procollagen (PIIINP). Defects in tenascin-X interfere in the deposition of collagen and elastin fibrils in dermis and cause a recessive form of classic EDS. , Type III collagen is synthesized by cells as a pre-procollagen.. Rather, the reactive interstitial fibrosis that occurs is the result of altered endocrine signaling. Type III collagen mutations are associated with Ehlers–Danlos syndrome, vascular deficiency, and aortic and arterial aneurysms. This recessive form of EDS type VII is characterized by deficiency of the N-terminal proteinase. Unlearning at least part of what the textbooks say", 10.1002/(SICI)1098-1004(1997)9:4<300::AID-HUMU2>3.0.CO;2-9, "Diagnosis, natural history, and management in vascular Ehlers-Danlos syndrome", "Crystal structure of human type III collagen Gly991-Gly1032 cystine knot-containing peptide shows both 7/2 and 10/3 triple helical symmetries", "Characterization of human type III collagen expressed in a baculovirus system. Furthermore, studies indicate that genetic and epigenetic aberrations that result in changes in expression levels of MMP-1, MMP-8, and MMP-9 are linked to preterm premature rupture of membranes (PPROM) and preterm birth, underscoring their important role (Ferrand et al., 2002; Wang et al., 2004, 2008). Production of a protein with a stable triple helix requires coexpression with the two types of recombinant prolyl 4-hydroxylase subunit", https://en.wikipedia.org/w/index.php?title=Collagen,_type_III,_alpha_1&oldid=984348032, Wikipedia articles with corresponding academic peer reviewed articles, Wikipedia articles with corresponding articles published in Gene, Creative Commons Attribution-ShareAlike License, This page was last edited on 19 October 2020, at 17:07. the rate of ongoing fibrosis) rather than the absolute amount of fibrosis present in the liver. Affected individuals have a significant risk of acute vascular ruptures and death. The proportion of this pN-collagen is higher than for type I collagen, as practically all type III collagen fibers possess an outside layer of pN-collagen. In addition, muscle cramps and pain as well as distal atrophy, and abnormal muscle imaging findings have been described (91). Second, some of the lysine residues are hydroxylated or glycosylated, and some lysine as well as hydroxylysine residues undergo oxidative deamination catalysed by lysyl oxidase. After passing through the Golgi apparatus it is transported to the cell surface and secreted into the interstitium of the connective tissue.14 Here occur cleavage of the terminal extensions of procollagen and the subsequent crosslinking of molecules to form stable collagen.15 Collagen appears to be turned over continuously; its degradation is brought about by collagenase. The fourth mouse model with defective Col3a1 gene is the tight skin mouse (Tsk2/+), which resembles the human systemic sclerosis. It is also found in many other tissues together with type I collagen. Peptides: Type I and Type III Collagen. Type III is abundant in the intestines.  This refers to a situation where one of the parents carries the mutation in some, but not all of her or his cells, and appears phenotypically healthy, but has more than one affected offspring. Both are found in the endo-, epi-, and perimyseum in muscle. Quantitatively, types I and III collagen are involved in hepatic fibrosis but type IV is also important in basement membranes. Also, raised bradykinin levels in aldosterone–salt excess may also stimulate increased collagen deposition in the heart. While it has been shown that inflammation in response to infection can result in elevated MMP activity, the potential role of bacterial collagenases has not been investigated. In addition, rodent models indicate that the effect of aldosterone on cardiac fibrosis is critically dependent on salt status; animals infused with aldosterone on a restricted salt diet do not have a fibrosis of the heart. Four different mouse models with Col3a1 defects have been reported. Another study discovered mice with a naturally occurring large deletion of the Col3a1 gene. They are also found in traditional bone broths, particularly when you include the … The COL3A1 gene is located on the long (q) arm of chromosome 2 at 2q32.2, between positions 188,974,372 and 189,012,745. M.J. Nielsen, M.A. Also, the major triple helical domain, 1029 residues in humans, is a little longer than the same domain in type I and II collagen molecules containing 1014 residues.
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