Hi,
I may be way off track here (science is not my strong point) but does anyone out there know if the protein 'Beta Spectrin' is present in corneal nerve cells?
I only ask this after reading a recent article that has discovered that the absence of the protein may be the cause for general nerve fibers to lose their flexibility and break.
I guess what I asking is if the nerve fibers present in the cornea have any relation at all to its flexability (Structural integrity)? If they do then would not the lack of these proteins result in a slackening (for want of a better word) of the corneal surface? Like a rubber band that has been overstretched and no longer maintains its original structure.
Could this in any way be a contributing factor toward keratoconus?
I'm way out of my depth with this kind of technical discussion... so I welcome any re-education on this point
Hari
Beta Spectrin
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- Hari Navarro
- Regular contributor
- Posts: 112
- Joined: Fri 26 Mar 2004 9:52 pm
- Keratoconus: Yes, I have KC
- Vision: Other
- Location: New Zealand
- Hari Navarro
- Regular contributor
- Posts: 112
- Joined: Fri 26 Mar 2004 9:52 pm
- Keratoconus: Yes, I have KC
- Vision: Other
- Location: New Zealand
Re: Beta Spectrin
I thought this was of further interest as it seems there has already been discussion as to the possibility of corneal nerves having direct effect on keratoconus progression. The article does not discuss beta spectrin but is it not possible that (if it is indeed present) this particular proteins absence would create a destabilising effect?
SOURCE: Brookes NH, Loh IP, Clover GM, et al. Involvement of corneal nerves in the progression of keratoconus. Exp Eye Res 2003;77(4):515-24.
Hari
Involvement of Corneal Nerves in the Progression of Keratoconus
Researchers at the University of Auckland, New Zealand, believe that studying the process of extracellular matrix remodeling from studies of connective tissues other than the cornea and from wound healing studies in the cornea can provide insight into the molecular mechanisms of keratoconic disease pathogenesis and progression.
The researchers previously developed a new approach to studying keratoconus based on the observation that there is a gradient of damage across the keratoconic cone. They identified a number of cellular characteristics of keratoconus, such as discrete incursions of fine cellular processes from the anterior keratocytes in association with localized indentation of the basal epithelium, and increased levels of the lysosomal enzymes Cathepsin B and G in aberrant keratocytes, located beneath compromised regions of Bowman's layer and deeper in the stroma. Enzyme activity by these cells appeared to cause localized structural degradation of the anterior stroma, leading to near-complete destruction of Bowman's layer and the stroma. This often necessitated a full-thickness corneal graft for sight restoration. The current study extended their initial findings by investigating the role of corneal nerves passing between the stroma and epithelium at the sites of early degradative change observed previously.
Cells in sections of normal and keratoconic human corneas were labeled with the fixable fluorescent viability dye 5-chloromethylfluorescein diacetate, antibodies to alpha-tubulin (nerves), alpha3beta1 integrin, Cathepsin B and G and the nuclear dye DAPI. They were then examined with a confocal microscope. Anterior keratocyte nuclei were seen wrapping around the nerves as they passed through the otherwise acellular Bowman's layer, and as the disease progressed and Bowman's layer degraded, these keratocytes expressed higher levels of Cathepsin B and G, and became displaced anteriorly into to the epithelium. Localized nerve thickenings also developed within the epithelium in association with Cathepsin B and G expression, and appeared to be very destructive to the cornea. The authors believe that additional studies will help determine how well this model fits the actual molecular basis of the pathogenesis of keratoconus.
SOURCE: Brookes NH, Loh IP, Clover GM, et al. Involvement of corneal nerves in the progression of keratoconus. Exp Eye Res 2003;77(4):515-24.
Hari
- David Bennett
- Optometrist
- Posts: 34
- Joined: Tue 03 Feb 2004 3:32 pm
- Location: Nottingham, UK
Re: Beta Spectrin
That's stunning research! WOW!!!
With this stuff going on in 10 years it may be possible to really help and solve the progression of KC. These guys need lots of money!
Best
David
With this stuff going on in 10 years it may be possible to really help and solve the progression of KC. These guys need lots of money!
Best
David
David Bennett Bsc(Hons) MCOptom
The Courtyard
28 The ropewalk
Nottingham NG1 5DW
T: 0115 947 6309
F: 0115 958 6971
The Courtyard
28 The ropewalk
Nottingham NG1 5DW
T: 0115 947 6309
F: 0115 958 6971
- John Smith
- Moderator
- Posts: 1941
- Joined: Thu 08 Jan 2004 12:48 am
- Keratoconus: Yes, I have KC
- Vision: Graft(s) and spectacles
- Location: Sidcup, Kent
Re: Beta Spectrin
Hi Hari,
I can't say I understand most of that, but it certainly sounds interesting. Can anyone (David?) translate for us laymen?
I can't say I understand most of that, but it certainly sounds interesting. Can anyone (David?) translate for us laymen?
John
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