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Membrane type-1 matrix metalloproteinases and tissue inhibitor of metalloproteinases-2 RNA levels mimic each other during Xenopus laevis metamorphosis.

Walsh LA, Carere DA, Cooper CA, Damjanovski S - PLoS ONE (2007)

Bottom Line: Here, using RT-PCR analysis, we examine the metamorphic RNA levels of two membrane-type MMPs (MT1-MMP, MT3-MMP), two TIMPs (TIMP-2, TIMP-3) and a potent gelatinase (Gel-A) that can be activated by the combinatory activity of a MT-MMP and a TIMP.In the metamorphic tail and intestine the RNA levels of TIMP-2 and MT1-MMP mirror each other, and closely resemble that of Gel-A as all three are elevated during periods of cell death and proliferation.Intriguingly, TIMP-3, which has been shown to have anti-apoptotic activity, is found at low levels in tissues during periods of apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of Western Ontario, London, Ontario, Canada.

ABSTRACT
Matrix metalloproteinases (MMPs) and their endogenous inhibitors TIMPs (tissue inhibitors of MMPs), are two protein families that work together to remodel the extracellular matrix (ECM). TIMPs serve not only to inhibit MMP activity, but also aid in the activation of MMPs that are secreted as inactive zymogens. Xenopus laevis metamorphosis is an ideal model for studying MMP and TIMP expression levels because all tissues are remodeled under the control of one molecule, thyroid hormone. Here, using RT-PCR analysis, we examine the metamorphic RNA levels of two membrane-type MMPs (MT1-MMP, MT3-MMP), two TIMPs (TIMP-2, TIMP-3) and a potent gelatinase (Gel-A) that can be activated by the combinatory activity of a MT-MMP and a TIMP. In the metamorphic tail and intestine the RNA levels of TIMP-2 and MT1-MMP mirror each other, and closely resemble that of Gel-A as all three are elevated during periods of cell death and proliferation. Conversely, MT3-MMP and TIMP-3 do not have similar RNA level patterns nor do they mimic the RNA levels of the other genes examined. Intriguingly, TIMP-3, which has been shown to have anti-apoptotic activity, is found at low levels in tissues during periods of apoptosis.

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Related in: MedlinePlus

Schematic of Intestinal and Tail Cell Death and Cell Proliferation Events During Metamorphosis.Xenopus laevis metamorphosis begins when T3 levels elevate at stage 57 and terminates at stage 66 [26]. Top illustrations are of intestine cross-sections and are not to scale. Distances between stages are also not to scale. In response to T3 the intestine changes from a simple structure with one luminal fold (stage 56) to one with multiple folds in the post-metamorphic froglet following stage 66. As intestine metamorphosis begins ECM remodeling in the connective tissue (C) results in cell death (open circles) and cell proliferation (closed circles) of overlying epithelial cells (E). Bottom illustrations represent tail lengths during metamorphosis. Tail regression due to cell death begins at stage 62/63 and is complete by stage 66. Solid line = cell death, dashed line = cell proliferation. C = connective tissue, E = epithelial, M = muscle
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pone-0001000-g001: Schematic of Intestinal and Tail Cell Death and Cell Proliferation Events During Metamorphosis.Xenopus laevis metamorphosis begins when T3 levels elevate at stage 57 and terminates at stage 66 [26]. Top illustrations are of intestine cross-sections and are not to scale. Distances between stages are also not to scale. In response to T3 the intestine changes from a simple structure with one luminal fold (stage 56) to one with multiple folds in the post-metamorphic froglet following stage 66. As intestine metamorphosis begins ECM remodeling in the connective tissue (C) results in cell death (open circles) and cell proliferation (closed circles) of overlying epithelial cells (E). Bottom illustrations represent tail lengths during metamorphosis. Tail regression due to cell death begins at stage 62/63 and is complete by stage 66. Solid line = cell death, dashed line = cell proliferation. C = connective tissue, E = epithelial, M = muscle

Mentions: Amphibian metamorphosis is a late developmental event that has been used to examine numerous processes including; cell signaling, receptor function, gene regulation, morphogenesis, and effects of environmental toxins [1]–[4]. While intricate, the entire metamorphic process is controlled by one molecule, thyroid hormone (T3). During Xenopus laevis metamorphosis all tissues are altered in some way, where structures are either created de novo (such as the limbs), removed completely (such as the tail), or remodeled (skin, the head and gills, and internal organs such as the intestine amongst others). This T3 dependent process is exemplified in the intestine (Figure 1) where embryonic epithelial cell death and adult epithelial cell proliferation facilitate the metamorphoses of an herbivorous tadpole into an omnivorous frog [5]. Removal of the tail, on the other hand, is achieved largely through apoptotic events late in the metamorphic process (Figure 1). While the ECM remodeling in both of these organs is facilitated by a similar array of molecules [6]–[9], the different cellular responses (proliferation vs. death) to this remodeling allow for the investigation of the possible functions of the molecules that remodel the ECM.


Membrane type-1 matrix metalloproteinases and tissue inhibitor of metalloproteinases-2 RNA levels mimic each other during Xenopus laevis metamorphosis.

Walsh LA, Carere DA, Cooper CA, Damjanovski S - PLoS ONE (2007)

Schematic of Intestinal and Tail Cell Death and Cell Proliferation Events During Metamorphosis.Xenopus laevis metamorphosis begins when T3 levels elevate at stage 57 and terminates at stage 66 [26]. Top illustrations are of intestine cross-sections and are not to scale. Distances between stages are also not to scale. In response to T3 the intestine changes from a simple structure with one luminal fold (stage 56) to one with multiple folds in the post-metamorphic froglet following stage 66. As intestine metamorphosis begins ECM remodeling in the connective tissue (C) results in cell death (open circles) and cell proliferation (closed circles) of overlying epithelial cells (E). Bottom illustrations represent tail lengths during metamorphosis. Tail regression due to cell death begins at stage 62/63 and is complete by stage 66. Solid line = cell death, dashed line = cell proliferation. C = connective tissue, E = epithelial, M = muscle
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC1991586&req=5

pone-0001000-g001: Schematic of Intestinal and Tail Cell Death and Cell Proliferation Events During Metamorphosis.Xenopus laevis metamorphosis begins when T3 levels elevate at stage 57 and terminates at stage 66 [26]. Top illustrations are of intestine cross-sections and are not to scale. Distances between stages are also not to scale. In response to T3 the intestine changes from a simple structure with one luminal fold (stage 56) to one with multiple folds in the post-metamorphic froglet following stage 66. As intestine metamorphosis begins ECM remodeling in the connective tissue (C) results in cell death (open circles) and cell proliferation (closed circles) of overlying epithelial cells (E). Bottom illustrations represent tail lengths during metamorphosis. Tail regression due to cell death begins at stage 62/63 and is complete by stage 66. Solid line = cell death, dashed line = cell proliferation. C = connective tissue, E = epithelial, M = muscle
Mentions: Amphibian metamorphosis is a late developmental event that has been used to examine numerous processes including; cell signaling, receptor function, gene regulation, morphogenesis, and effects of environmental toxins [1]–[4]. While intricate, the entire metamorphic process is controlled by one molecule, thyroid hormone (T3). During Xenopus laevis metamorphosis all tissues are altered in some way, where structures are either created de novo (such as the limbs), removed completely (such as the tail), or remodeled (skin, the head and gills, and internal organs such as the intestine amongst others). This T3 dependent process is exemplified in the intestine (Figure 1) where embryonic epithelial cell death and adult epithelial cell proliferation facilitate the metamorphoses of an herbivorous tadpole into an omnivorous frog [5]. Removal of the tail, on the other hand, is achieved largely through apoptotic events late in the metamorphic process (Figure 1). While the ECM remodeling in both of these organs is facilitated by a similar array of molecules [6]–[9], the different cellular responses (proliferation vs. death) to this remodeling allow for the investigation of the possible functions of the molecules that remodel the ECM.

Bottom Line: Here, using RT-PCR analysis, we examine the metamorphic RNA levels of two membrane-type MMPs (MT1-MMP, MT3-MMP), two TIMPs (TIMP-2, TIMP-3) and a potent gelatinase (Gel-A) that can be activated by the combinatory activity of a MT-MMP and a TIMP.In the metamorphic tail and intestine the RNA levels of TIMP-2 and MT1-MMP mirror each other, and closely resemble that of Gel-A as all three are elevated during periods of cell death and proliferation.Intriguingly, TIMP-3, which has been shown to have anti-apoptotic activity, is found at low levels in tissues during periods of apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of Western Ontario, London, Ontario, Canada.

ABSTRACT
Matrix metalloproteinases (MMPs) and their endogenous inhibitors TIMPs (tissue inhibitors of MMPs), are two protein families that work together to remodel the extracellular matrix (ECM). TIMPs serve not only to inhibit MMP activity, but also aid in the activation of MMPs that are secreted as inactive zymogens. Xenopus laevis metamorphosis is an ideal model for studying MMP and TIMP expression levels because all tissues are remodeled under the control of one molecule, thyroid hormone. Here, using RT-PCR analysis, we examine the metamorphic RNA levels of two membrane-type MMPs (MT1-MMP, MT3-MMP), two TIMPs (TIMP-2, TIMP-3) and a potent gelatinase (Gel-A) that can be activated by the combinatory activity of a MT-MMP and a TIMP. In the metamorphic tail and intestine the RNA levels of TIMP-2 and MT1-MMP mirror each other, and closely resemble that of Gel-A as all three are elevated during periods of cell death and proliferation. Conversely, MT3-MMP and TIMP-3 do not have similar RNA level patterns nor do they mimic the RNA levels of the other genes examined. Intriguingly, TIMP-3, which has been shown to have anti-apoptotic activity, is found at low levels in tissues during periods of apoptosis.

Show MeSH
Related in: MedlinePlus