Treatment of Radiation Injury

Akita, Sadanori

doi:10.1089/wound.2012.0403

Cited by 39 publications

(29 citation statements)

References 63 publications

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“…2C). 19 Interestingly, SMG from the 39-year-old female patient (patient 4) displayed high levels of collagen deposition (although less than patient 3), which appears to be typical of early radiation stages 20 …”

Section: Gamma Irradiation Causes Collagen Deposition In Human Smgmentioning

confidence: 99%

Post-Irradiated Human Submandibular Glands Display High Collagen Deposition, Disorganized Cell Junctions, and an Increased Number of Adipocytes

Nam

Maruyama

Trump

et al. 2016

J Histochem Cytochem.

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Salivary glands are vital for maintaining oral health. Head and neck radiation therapy is one of the most common causes of salivary gland hypofunction. Little is known about the structural changes that occur in salivary glands after radiation therapy. The aim of this study is to understand the structural changes that occur in post-irradiated human (submandibular gland [SMG]) as compared with untreated ones. We determined changes in epithelial polarity, presence of collagen deposition, and alteration in adipose tissue. We used formalin-fixed paraffin-embedded human SMG from two female subjects exposed to head and neck irradiation. We utilized hematoxylin and eosin staining and Masson’s Trichrome staining. The immunostained tissue sections were examined using confocal microscopy. The number and size of adipocytes per tissue section were calculated using ImageJ, Prism, and SPSS software. Post-irradiated human SMG displayed high collagen deposition, disorganized cell junctions, and an increased number of adipocytes as compared with non-irradiated controls. These findings are important to improve our understanding of the individual risk and variation in radiation-related salivary gland dysfunction.

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Section: Gamma Irradiation Causes Collagen Deposition In Human Smgmentioning

confidence: 99%

Post-Irradiated Human Submandibular Glands Display High Collagen Deposition, Disorganized Cell Junctions, and an Increased Number of Adipocytes

Nam

Maruyama

Trump

et al. 2016

J Histochem Cytochem.

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“…By day 42 after irradiation, Smad3 −/− mice showed significant improvement in limb excursion compared with wild-type mice. The initial decrease in limb excursion observed in Smad3 −/− mice was most likely due to edema, which is observed postirradiation [24]. Smad3 −/− mice showed no detectable RF in tissues examined out to 100 days in later stages [22,23].…”

Section: Quantitation Of Parameters Of Radiation-induced Hind Limb Fimentioning

confidence: 99%

Adipose-Derived Stem Cell Therapy Ameliorates Ionizing Irradiation Fibrosis via Hepatocyte Growth Factor-Mediated Transforming Growth Factor-β Downregulation and Recruitment of Bone Marrow Cells

et al. 2019

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Radiation therapy to anatomic regions, including the head and neck, chest wall, and extremities, can produce radiation‐induced fibrosis (RIF). To elucidate the cellular and molecular mechanism(s) involved in RIF, female C57BL/6J mice were irradiated to the right flank to 35 Gy in single fraction using 6 Mv electrons. Radiation fibrosis was detected by day 14, was increased by day 28, and confirmed by Masson's trichrome histological staining for collagen. Biopsied tissue at day 14 showed an increase in expression of fibrosis‐related genes including transforming growth factor‐β (TGF‐β) and collagens 1–6. A single adipose‐derived stem cell (ASC) injection on day 28 at the irradiated site decreased by day 40: epithelial thickness, collagen deposition, and significantly improved limb excursion compared with irradiated controls. Noncontact transwell coculture of ASCs above a monolayer of irradiated human foreskin fibroblasts downregulated fibrosis‐related genes TGF‐β, connective tissue growth factor, interleukin‐1, NF‐kB, tumor necrosis factor, and collagens 1–6. Hepatocyte growth factor (HGF) secreted by ASCs was identified as a novel mechanism by which ASCs exert antifibrotic effects by downregulating fibrotic gene expression in irradiated cells and recruiting bone marrow cells to the irradiated site. In conclusion, these data indicate a mechanistic role of HGF secreted by ASCs in reducing RIF. Stem Cells 2019;37:791–802

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“…They identified a SNP associated with the FSHR gene that encodes the follicle stimulating hormone receptor, which is involved in gonad development and function 20 . SNPs causing ED were found to be significantly associated with adverse reactions in patients treated with RT 21, 22. The predictive systems for cancer drug resistance, responses to RT or radiochemotherapy, and cellular toxicity to RT has shown great promise in advancement of radiogenomic cancer research 23 …”

Section: History Of Ed Treatmentmentioning

confidence: 99%

Radiation-induced erectile dysfunction: Recent advances and future directions

Mahmood

Shamah

Creed

et al. 2016

Advances in Radiation Oncology

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Prostate cancer is one of the most prevalent cancers and the second leading cause of cancer-related deaths in men in the United States. A large number of patients undergo radiation therapy (RT) as a standard care of treatment; however, RT causes erectile dysfunction (radiation-induced erectile dysfunction; RiED) because of late side effects after RT that significantly affects quality of life of prostate cancer patients. Within 5 years of RT, approximately 50% of patients could develop RiED. Based on the past and current research findings and number of publications from our group, the precise mechanism of RiED is under exploration in detail. Recent investigations have shown prostate RT induces significant morphologic arterial damage with aberrant alterations in internal pudendal arterial tone. Prostatic RT also reduces motor function in the cavernous nerve which may attribute to axonal degeneration may contributing to RiED. Furthermore, the advances in radiogenomics such as radiation induced somatic mutation identification, copy number variation and genome-wide association studies has significantly facilitated identification of biomarkers that could be used to monitoring radiation-induced late toxicity and damage to the nerves; thus, genomic- and proteomic-based biomarkers could greatly improve treatment and minimize arterial tissue and nerve damage. Further, advanced technologies such as proton beam therapy that precisely target tumor and significantly reduce off-target damage to vital organs and healthy tissues. In this review, we summarize recent advances in RiED research and novel treatment modalities for RiED. We also discuss the possible molecular mechanism involved in the development of RiED in prostate cancer patients. Further, we discuss various readily available methods as well as novel strategies such as stem cell therapies, shockwave therapy, nerve grafting with tissue engineering, and nutritional supplementations might be used to mitigate or cure sexual dysfunction following radiation treatment.

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Treatment of Radiation Injury

Cited by 39 publications

References 63 publications

Post-Irradiated Human Submandibular Glands Display High Collagen Deposition, Disorganized Cell Junctions, and an Increased Number of Adipocytes

Post-Irradiated Human Submandibular Glands Display High Collagen Deposition, Disorganized Cell Junctions, and an Increased Number of Adipocytes

Adipose-Derived Stem Cell Therapy Ameliorates Ionizing Irradiation Fibrosis via Hepatocyte Growth Factor-Mediated Transforming Growth Factor-β Downregulation and Recruitment of Bone Marrow Cells

Radiation-induced erectile dysfunction: Recent advances and future directions

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