Education and demonstration – Means for demonstrating apparatus – product – or surface... – Manually manipulated pin or peg inserted into display board
Reexamination Certificate
2002-04-11
2004-03-30
Bodson, Shelley A. (Department: 1616)
Education and demonstration
Means for demonstrating apparatus, product, or surface...
Manually manipulated pin or peg inserted into display board
C424S400000, C514S937000
Reexamination Certificate
active
06712617
ABSTRACT:
BACKGROUND OF THE INVENTION
Photoaging due to chronic exposure to ultraviolet-B (UVB) irradiation results, inter alia, in the formation of wrinkles.
SUMMARY OF THE INVENTION
The invention is based, in part, on the discovery that inhibition of skin angiogenesis can prevent UVB-induced skin damage, e.g., long term (chronic) UVB induced photoaging, e.g., wrinkle formation, in vivo, in mammals, e.g., humans.
Accordingly, the invention features a method preventing or treating long-term UVB-induced skin damage, e.g., wrinkles, in a subject. The method includes inhibiting angiogenesis in the skin of the subject. In a preferred embodiment, angiogenesis is inhibited before or at the time of a UVB exposure.
In a preferred embodiment, the method also includes identifying a subject, e.g., a mammal, e.g., a human or a non-human mammal, at risk of long term UVB-induced skin damage. The identification of a subject at risk for long term UVB-induced skin damage, e.g., wrinkles, can be performed e.g., by the subject, by a health care provider, or by a provider of cosmetics. The inhibition of angiogenesis can be performed, e.g., by the subject, by a health care provider, or by a provider of cosmetics.
In a preferred embodiment the subject is at least 5 years of age. Preferably, the subject is at least 10, 15, 20, 25, 30, 35, 40, 45, 50, or more years of age.
In a preferred embodiment, wrinkle formation is prevented or reduced.
In a preferred embodiment, angiogenesis is inhibited by increasing the activity of one or more anti-angiogenic factors, e.g., increasing the activity of naturally occurring anti-angiogenic proteins such as TSP-2 or TSP-1 in the subject, thereby preventing wrinkle formation. TSP-2 activity can be increased, e.g., by administering an agent which increases a TSP-2 activity. In a preferred embodiment, an agent which increases a TSP-2 activity can be one or more of the following: a TSP-2 polypeptide, or a biologically active fragment or analog thereof, e.g., a TSP-2 derived polypeptide or retro-inverso polypeptide thereof; a nucleic acid encoding a TSP-2 polypeptide, or a biologically active fragment or analog thereof; an agonist of TSP-2, e.g., an antibody or a small molecule having or increasing TSP-2 activity; or an agent that increases TSP-2 nucleic acid expression, e.g., a small molecule which binds to the promoter region of TSP-2 and increases expression.
In a preferred embodiment, TSP-2 is increased by an agent, e.g., a small molecule, which induces TSP-2 expression. Examples of agents that can induce expression of TSP-2 include fetal calf serum and TGF-&agr;. In preferred embodiments, an agent that induces TSP-2 expression is administered topically. In preferred embodiments, the agent is administered to a subject sufficiently before UVB exposure, e.g., sun exposure, such that an anti-angiogenesis effect is present in the subject's skin at the time of UVB exposure.
TSP-2 activity can also be increased by controlled delivery to the subject of a TSP-2 nucleic acid, or a TSP-2 protein, fragment, or analog. A TSP-2 nucleic acid, protein, fragment, or analog can be administered to the subject in combination with a controlled release device, e.g., a biocompatible polymer, micro particle, or mesh. The device can reduce degradation and control the release of the TSP-2 nucleic acid, protein, fragment, or analog. Such a TSP-2 biocompatible controlled release system can be administered to the subject, e.g., by injection or implantation, e.g., intramuscularly, subcutaneously, intravenously, or at an organ, joint cavity, or at a lesion.
The level of TSP-2 can also be increased by increasing the endogenous TSP-2 activity. Activity can be increased by increasing the level of expression of the gene, e.g., by increasing transcription of the TSP-2 gene; increasing the stability of the TSP-2 mRNA, e.g., by altering the secondary or tertiary structure of the mRNA; increasing the translation of TSP-2 mRNA, e.g., by altering the sequence of the TSP-2 mRNA; and/or increasing the stability of the TSP-2 protein. Transcription of the TSP-2 gene can be increased, e.g., by altering the regulatory sequences of the endogenous TSP-2 gene. In one embodiment the regulatory sequence can be altered by: the addition of a positive regulatory element (such as an enhancer or a DNA-binding site for a transcriptional activator); the deletion of a negative regulatory element (such as a DNA-binding site for a transcriptional repressor) and/or replacement of the endogenous regulatory sequence, or elements therein, with that of another gene, thereby allowing the TSP-2 gene to be transcribed more efficiently.
In a preferred embodiment, the agent is a compound, e.g., small molecule, which induces TSP-2.
TSP-1 activity can be increased, e.g., by administering an agent which increases a TSP-1 activity. In a preferred embodiment, an agent which increases a TSP-1 activity can be one or more of the following: a TSP-1 polypeptide, or a biologically active fragment or analog thereof, e.g., a TSP-1 derived polypeptide or retro-inverso polypeptide thereof; a nucleic acid encoding a TSP-1 polypeptide, or a biologically active fragment or analog thereof; an agonist of TSP-1, e.g., an antibody or a small molecule having or increasing TSP-1 activity; or an agent that increases TSP-1 nucleic acid expression, e.g., a small molecule which binds to the promoter region of TSP-1 and increases expression.
In a preferred embodiment, TSP-1 is increased by an agent, e.g., a small molecule, which induces TSP-1 expression. Examples of agents that can induce expression of TSP-1 include fetal calf serum and TGF-&agr;. In preferred embodiments, an agent that induces TSP-1 expression is administered topically. In preferred embodiments, the agent is administered to a subject sufficiently before UVB exposure, e.g., sun exposure, such that an anti-angiogenesis effect is present in the subject's skin at the time of UVB exposure.
TSP-1 activity can also be increased by controlled delivery to the subject of a TSP-1 nucleic acid, or a TSP-1 protein, fragment, or analog. A TSP-1 nucleic acid, protein, fragment, or analog can be administered to the subject in combination with a controlled release device, e.g., a biocompatible polymer, micro particle, or mesh. The device can reduce degradation and control the release of the TSP-1 nucleic acid, protein, fragment, or analog. Such a TSP-1 biocompatible controlled release system can be administered to the subject, e.g., by injection or implantation, e.g., intramuscularly, subcutaneously, intravenously, or at an organ, joint cavity, or at a lesion.
The level of TSP-1 can also be increased by increasing the endogenous TSP-1 activity. Activity can be increased by increasing the level of expression of the gene, e.g., by increasing transcription of the TSP-1 gene; increasing the stability of the TSP-1 mRNA, e.g., by altering the secondary or tertiary structure of the mRNA; increasing the translation of TSP-1 mRNA, e.g., by altering the sequence of the TSP-1 mRNA; and/or increasing the stability of the TSP-1 protein. Transcription of the TSP-1 gene can be increased, e.g., by altering the regulatory sequences of the endogenous TSP-1 gene. In one embodiment the regulatory sequence can be altered by: the addition of a positive regulatory element (such as an enhancer or a DNA-binding site for a transcriptional activator); the deletion of a negative regulatory element (such as a DNA-binding site for a transcriptional repressor) and/or replacement of the endogenous regulatory sequence, or elements therein, with that of another gene, thereby allowing the TSP-1 gene to be transcribed more efficiently.
In a preferred embodiment, the agent is a compound, e.g., small molecule, which induces TSP-1.
In a preferred embodiment, the agent which increases the activity of one or more anti-angiogenic factors, e.g., by inducing the activity of a naturally occurring anti-angiogenic protein such as TSP-2 or TSP-1 is administered, e.g., by topically administering the agent; systemically administering the agent; orally administ
Detmar Michael J.
Yano Kiichiro
Bodson Shelley A.
Fish & Richardson PC
The General Hospital Corporation
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