TY - JOUR
T1 - Melanophores in damselfish neurofibromatosis
T2 - Alterations in morphology and melanosome aggregation responses
AU - Schmale, Michael C.
AU - Kemerer, Timothy W.
N1 - Funding Information:
The authors thank Lynne Fieber and Patrick Walsh for critical review of the manuscript and Saul Cacal for assistance with preparation of cell cultures. In addition, we thank the personnel of the Biscayne National Park (National Park Service) and the Key Largo National Marine Sanctuary, National Oceanic and Atmospheric Administration (research conduct- ed under permits KLNMS and LKNMS 2-86, 3-88, 5-89, and 1-91). This research was supported by Pub-lic Health Service grants NS21997, CA53313, and P30 ES05705.
PY - 1996/3
Y1 - 1996/3
N2 - Damselfish neurofibromatosis (DNF) is a neoplastic disease affecting bicolor damselfish Pomacentrus partitus on south Florida reefs. This disease exhibits many traits in common with neurofibromatosis type-1 in humans, including multiple plexiform neurofibromas and areas of hyperpigmentation. An important issue in understanding the pathogenesis of DNF is the relation between chromatophores and other cell types that give rise to tumors in this disease. Melanophores cultured from tumors of fish with DNF were compared in vitro with cells from normal skin of healthy fish to determine if these cells were morphologically or physiologically altered in this disease. Melanophores from tumors were significantly larger in cross-sectional perimeter and area than normal counterparts. Pigment translocation responses were measured by bath application of norepinephrine. At drug concentrations of 5 × 10-9 to 5 × 10-5 significantly fewer tumorderived cells than normal cells exhibited complete melanosome aggregation, and mean response times for tumor-derived cells were significantly longer. Aggregation times were not positively correlated with cell perimeter or surface area for either cell type. Two types of response fatigue were observed with repeated exposure protocols. A loss of ability to spontaneously disperse pigment after repeated aggregations induced by high doses of norepinephrine (5 × 10-5 M) was observed in both normal and tumor-derived melanophores. In contrast, at lower concentrations of norepinephrine (5 × 10-7 M), an increasing proportion of tumor-derived, but not normal cells, failed to aggregate pigment as exposures were repeated. However, fatigue affected only the degree of pigment aggregation and not the rate of melanosome movement. These data demonstrate that melanophores present in damselfish neurofibromatosis are significantly different from their healthy counterparts in both morphology and physiology in vitro. This system should be useful for understanding how the agent responsible for DNF alters either specific hormone receptors, second messenger pathways, pigment organelles, cytoskeletal components, mechanochemical events, or a combination of these factors in these cells.
AB - Damselfish neurofibromatosis (DNF) is a neoplastic disease affecting bicolor damselfish Pomacentrus partitus on south Florida reefs. This disease exhibits many traits in common with neurofibromatosis type-1 in humans, including multiple plexiform neurofibromas and areas of hyperpigmentation. An important issue in understanding the pathogenesis of DNF is the relation between chromatophores and other cell types that give rise to tumors in this disease. Melanophores cultured from tumors of fish with DNF were compared in vitro with cells from normal skin of healthy fish to determine if these cells were morphologically or physiologically altered in this disease. Melanophores from tumors were significantly larger in cross-sectional perimeter and area than normal counterparts. Pigment translocation responses were measured by bath application of norepinephrine. At drug concentrations of 5 × 10-9 to 5 × 10-5 significantly fewer tumorderived cells than normal cells exhibited complete melanosome aggregation, and mean response times for tumor-derived cells were significantly longer. Aggregation times were not positively correlated with cell perimeter or surface area for either cell type. Two types of response fatigue were observed with repeated exposure protocols. A loss of ability to spontaneously disperse pigment after repeated aggregations induced by high doses of norepinephrine (5 × 10-5 M) was observed in both normal and tumor-derived melanophores. In contrast, at lower concentrations of norepinephrine (5 × 10-7 M), an increasing proportion of tumor-derived, but not normal cells, failed to aggregate pigment as exposures were repeated. However, fatigue affected only the degree of pigment aggregation and not the rate of melanosome movement. These data demonstrate that melanophores present in damselfish neurofibromatosis are significantly different from their healthy counterparts in both morphology and physiology in vitro. This system should be useful for understanding how the agent responsible for DNF alters either specific hormone receptors, second messenger pathways, pigment organelles, cytoskeletal components, mechanochemical events, or a combination of these factors in these cells.
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U2 - 10.1577/1548-8667(1996)008<0001:MIDNAI>2.3.CO;2
DO - 10.1577/1548-8667(1996)008<0001:MIDNAI>2.3.CO;2
M3 - Article
AN - SCOPUS:5344229387
VL - 8
SP - 1
EP - 12
JO - Journal of Aquatic Animal Health
JF - Journal of Aquatic Animal Health
SN - 0899-7659
IS - 1
ER -