INSIGHTS | PERSPECTIVES
17 FEBRUARY 2017 • VOL 355 ISSUE 6326 693 SCIENCE
regions and very close to or at the surface
in the colder polar regions (4). The calculated ice coverage, estimated to be ~10% in
the near-surface layer, cannot explain the
observed water vapor from Ceres because
temperatures in the ice layer will be too low
for substantial sublimation of ice. However,
even small impacts will locally expose ice
to the surface and may create sporadic activity. At the same time, this process poses
the question of the stability of the ice layer:
Those impacts remove ice from the upper
surface layer, and the resulting water vapor
will eventually escape from Ceres. It is not
obvious how the ice can remain close to
the surface over geological time scales. The
problem is similar to the question of how
cometary activity is maintained, with little
ice found on the surface of cometary nuclei.
In spite of the different size and activity of
the bodies (cometary nuclei are only a few
kilometers in size, and the sublimation rate
per area is orders of magnitude higher than
for Ceres), the physical process behind the
solution of both problems may be the same.
De Sanctis et al. provide the first observations of organic material on Ceres, confirming the presence of such material in the
asteroid belt. Furthermore, because Ceres
is a dwarf planet that may still preserve internal heat from its formation period and
may even contain a subsurface ocean (16),
this opens the possibility that primitive life
could have developed on Ceres itself. It joins
Mars and several satellites of the giant planets in the list of locations in the solar system
that may harbor life. Future missions to asteroids, comets, and the outer solar system
may provide answers to the fundamental
questions concerning the origin of water
and organic material on Earth and the possible formation of prebiotic material and
primitive life in the outer solar system. j
1. F. Capaccioni et al., Science 347, aaa0628 (2015).
2. K.Altwegg etal.,
3. M. C. De Sanctis et al. , Science355, 719 (2017).
4. T.H.Prettyman, Science 355,55(2017).
5. K. J. Walsh, A. Morbidelli, S. N. Raymond, D. P. O’Brien, A. M.
Mandell, Meteorit. Planet. Sci. 47, 1941 (2012).
6. M. J. Drake, K. Righter,Nature 416, 39 (2002).
7. A. Morbidelli et al ., Meteorit. Planet. Sci.35, 1309 (2000).
8. P. Hartogh etal .,Nature 478, 218 (2011).
9. D.Jewitt, Astron.J. 143,66(2012).
10. H. Campins et al., Nature 464, 1320 (2010).
11. A. F. Rivkin, J. P. Emery, Nature 464, 1322 (2010).
12. J.Licandro etal.,
13. M. Küppers et al ., Nature 505, 525 (2014).
14. T.Platz etal.,Nature Astron. 1,A0007(2016).
15. J.-P.Combes et al., Science 353,aaf3010(2016).
16. T.B.McCord, J.Castillo-Rogez,A.Rivkin,Space Sci.Rev.
163, 63 (2011).
Enhanced color composite of Oxo crater, the only illuminated location on Ceres where water ice was found.
Elevation is exaggerated by a factor of 2.
By Charles K. F. Chan1 and
Michael T. Longaker1,2
Following cutaneous injury in adult mammals, one of two outcomes can occur: successful healing with scar formation or nonsuccessful healing and a chronic wound. In humans, scar formation can be classified in
terms of “normal scar” formation versus
pathologically increased fibrosis, as seen in
hypertrophic scarring and keloids (1). Although scarring does not look or function
like surrounding unwounded skin, it allows one to survive injury (and hence, procreate). However, extensive scarring from
burns and conditions such as scleroderma
or epidermolysis bulosa are not only unsightly but also contribute to substantial
morbidity owing to loss of
functionality in affected tissues and limbs. In the United
States alone, there are greater
than 50 million incisions and
lacerations each year, all of
which heal with some degree
of scarring (2). Thus, scarring represents an enormous
and growing medical burden
in our aging population. On
page 748 of this issue, Plikus
et al. (3) demonstrate that
scarring could be mitigated
by controlling fibroblast plasticity. This
has very exciting translational implications for treating scar formation during
A wound represents a complex physi-
ological niche with numerous cell types,
cytokines, and growth factors, as well as
low oxygen, and high lactate (4). Tradition-
ally, wound repair is thought to proceed
through three phases: inflammatory, pro-
liferative, and remodeling (1). The initial
inflammatory phase prevents blood loss
and infection and clears debris, while the
following proliferative phase supports the
proliferation and migration of keratino-
cytes to reseal the epithelium. During the
latter remodeling phase, adipocytes, fi-
broblasts, and extracellular matrix fill the
wounded area to form scars. But scars are
distinguished from adjacent normal skin
by color, texture, and a lack of hair follicles
and secondary elements such as sweat and
sebaceous glands. Unexpectedly, it was re-
cently found that hair follicle regeneration
in mouse wounds could be stimulated with
secreted factors of the fibroblast growth
factor (FGF) and Wingless (WNT) signal-
ing pathways (5). Plikus et al. now make
the important finding that hair follicles can
change the fate of myofibroblasts (a known
cellular player in scarring) into adipocytes
through a signaling pathway that depends
on bone morphogenetic pro-
tein (BMP). Therefore, com-
binatorial WNT, FGF, and
BMP treatment could present
a biphasic strategy for scar-
less wound healing by first
stimulating regrowth of hair
follicles that would then in-
duce differentiation of scar-
forming myofibroblasts into
adipocytes (see the figure).
Intriguingly, the authors
found that myofibroblasts
isolated from keloid patients
also could be induced to become adipocytes by exposure to BMP. This has important implications clinically and suggests
a potentially effective treatment route for
keloids, which are specific to humans and
represent pathologic scars that are notoriously difficult to treat because they never
stop “growing” and frequently recur even
after surgical removal. With these results,
Plikus et al. illustrate how a better understanding of the complex microenvironment
of wounds and the functional plasticity of
the cell lineages that contribute to wound
repair, could lead to therapies for the physically scarred.
Given the many cell types and signaling
pathways involved in wound healing, the
reprogramming of a myofibroblast into an
adipocyte may not immediately seem sur-
Fibroblasts become fat to
Pathologic scarring could be avoided by manipulating
1Institute for Stem Cell Biology and Regenerative Medicine,
Stanford University, Palo Alto, CA 94305, USA. 2Hagey
Laboratory for Pediatric Regenerative Medicine and
Department of Surgery, Stanford University, Palo Alto, CA
94305, USA. Email: firstname.lastname@example.org;
in our aging